Title of Invention: Methods for measurement of inhibition of c-Jun N-terminal kinase in skin Abstract: Provided herein are methods for evaluating the effect of 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof in a patient with an assay based on UVB-irradiation and phosphorylated c-Jun expression. The analyses allow for evaluation of dose-response and identification of patient populations who are sensitive to 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof. Detailed Description: Part general_description_paragraphs: This application is a divisional of U.S. application Ser. No. 14/969,744, filed Dec. 15, 2015, currently allowed, which claims the benefit of U.S. Provisional Application No. 62/092,531, filed Dec. 16, 2014, the contents of which are incorporated by reference herein in their entirety. Part 1. FIELD: Provided herein are methods for measuring the inhibition of c-Jun N-terminal kinase (JNK) in skin using immunohistochemistry. Further provided herein is an assay based on UVB-irradiation and measurement of phospho c-Jun (or phosphorylated c-Jun) immunoreactivity useful for evaluating dose-response relationships of 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide and identifying and selecting patient populations sensitive or insensitive to 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide. Part 2. BACKGROUND: The connection between abnormal protein phosphorylation and the cause or consequence of diseases has been known for over 20 years. Accordingly, protein kinases have become a very important group of drug targets. (See Cohen, Nature, 1:309-315 (2002), Gaestel et al. Curr. Med. Chem. 14: 2214-223 (2007); Grimminger et al. Nat. Rev. Drug Disc. 9(12):956-970 (2010)). Various protein kinase inhibitors have been used clinically in the treatment of a wide variety of diseases, such as cancer and chronic inflammatory diseases, including rheumatoid arthritis and psoriasis. (See Cohen, Eur. J. Biochem., 268:5001-5010 (2001); Protein Kinase Inhibitors for the Treatment of Disease: The Promise and the Problems, Handbook of Experimental Pharmacology, Springer Berlin Heidelberg, 167 (2005)). JNK is a ubiquitously expressed serine/threonine kinase belonging, together with ERK (extracellular-regulated kinase) and p38, to the family of mitogen-activated protein kinases (MAPKs). Kyriakis J M, Sci. STKE (48):pe1 (2000); Whitmarsh A J, et al. Sci. STKE (1):pe1 (1999); Schramek H, News Physiol. Sci. 17:62-7 (2002); Ichijo H, Oncogene 18(45):6087-93 (1999). MAPKs are important mediators of signal transduction from the cell surface to the nucleus, using phosphorylation cascades to generate a coordinated response by a cell to an external stimulus by phosphorylation of selected intracellular proteins, including transcription factors. Additionally, JNK also phosphorylates non-nuclear proteins, for example, IRS-1, and Bcl-2 family members. Davis R J, Trends Biochem. Sci. 9(11):470-473 (1994); Seger R et al., FASEB J.; 9(9):726-35 (1995); Fanger G R et al., Curr. Opin. Genet. Dev.; 7(1):67-74 (1997). The mitogen activated protein (MAP) kinases participate in the transduction of signals to the nucleus of the cell in response to extracellular stimuli. Examples of MAP kinases from the ERK p38 and JNK isoforms include but are not limited to, mitogen-activated protein kinase 1 (ERK2), mitogen-activated protein kinase 8 (JNK1), mitogen-activated protein kinase 9 (MAPK9 or JNK2), mitogen-activated protein kinase 10 (MAPK10 or JNK3) and mitogen-activated protein kinase 14 (MAPK14 or p38alpha). MAP kinases are a family of proline-directed serine/threonine kinases that mediate signal transduction from extracellular receptors or heat shock, osmotic stress, reactive oxidant species (ROS) or UV radiation. See Sridhar et al., Pharmaceutical Research, 17:11 1345-1353 (2000). MAP kinases are activated via the phosphorylation of theonine and tyrosine by upstream dual-specificity protein kinases, including MKK and MEKK kinases. Cell proliferation and differentiation have been shown to be under the regulatory control of multiple MAP kinase cascades. See Sridhar et al., Pharmaceutical Research, 17:11 1345-1353 (2000). As such, the MAP kinase pathway plays critical roles in a number of disease states. For example, defects in activities of MAP kinases have been shown to lead to aberrant cell proliferation and carcinogenesis. See Hu et al., Cell Growth Differ. 11:191-200 (2000); and Das et al., Breast Cancer Res. Treat. 40:141 (1996). Moreover, MAP kinase activity has also been implicated in insulin resistance associated with type-2 diabetes and obesity. See Virkamaki et al., J. Clin. Invest. 103:931-943 (1999). Changes in insulin resistance may have a direct impact on the metabolism of glucose and lipid in the liver contributing to the development of steatosis that may progress to liver fibrosis. See Vallerie et al. Science Translational Medicine 2(60): 1-7 (2010). Steatosis may develop in the presence of either saturated or unsaturated free fatty acids (FFA). FFA promote robust JNK activation in liver and excessive concentrations of FFA may lead to hepatocyte apoptosis. It has been reported that JNK2−/− mice are partially protected from steatosis and apoptosis by saturated FFA (e.g. stearic acid) but not by unsaturated FFA. Malhi et al. J. Biol. Chem. 281:12093-12101 (2006). JNK1−/− mice were not protected from FFA induced injury. The role of JNK1 and JNK2 has been studied in CDAA-fed mice that progressed from steatosis to steatohepatitis to hepatic fibrosis. Kodama et al., Gastroenterology 137:1467-1477 (2009). While both JNK1−/− and JNK2−/− mice developed steatosis, the JNK1−/− mice, but not JNK2−/− mice, were remarkably resistant to progression to hepatitis and fibrosis. Chimeric mice with JNK1−/− deletion restricted to bone marrow cells were similarly resistant to hepatitis and fibrosis implicating the activated Kupffer cell as a key trigger for disease progression beyond steatosis. Indeed, JNK1−/− macrophages do not express IL-1, IL-6, TNF and NO in response to LPS, and Kupffer cells derived from JNK1−/− mice or from wild-type mice and treated with JNK inhibitor SP600125 display reduced TNF, IL-6, and IL-1 expression in response to LPS. Sanchez-Tillo et al., J Biol Chem. 282(17):12566-73 (2007); Kodama et al., Gastroenterology 137:1467-1477 (2009)). Previous studies have measured levels of IL-10, TNF-α, and NO in cells exposed to UVB irradiation either with or without specific inhibitors, demonstrating that UVB induced the production of those proinflammatory mediators, purportedly via activation of the p38 MAPK signalling pathway. Mutou Y, Tsukimoto M, Homma T, Kojima S, Immune Response Pathways in Human Keratinocyte (HaCat) Cells are Induced by Ultraviolet B via p38 Mitogen-activated Protein Kinase Activation, J. Health Science 2010; 56(6):675-83. Additionally, the induction of c-Jun protein and phosphorylation after UV irradiation of human skin has been reported. Fisher G, Talwar H, Lin J, Lin P, McPhillips F, Wang Z, Li X, Wan Y, Kang S, and Voorhees J, Retinoic Acid Inhibits Induction of c-Jun Protein by Ultraviolet Radiation That Occurs Subsequent To Activation Of Mitogen-Activated Protein Kinase Pathways In Human Skin In Vivo, J. Clin Invest. 1998; 101(6): 1432-40 and Einspahr J, Bowden T, Alberts D, McKenzie N, Saboda K, Warneke J, Salasche S, Ranger-Moore J, Lewandrowski C, Nagle R, Nickoloff B, Brooks, C, Dong Z, and Stratton S, Cross-Validation of Murine UV Signal Transduction Pathaways in Human Skin, Photochem. Photobiol. 2008; 84(2):463-76. Clinical markers are needed to evaluate the biological effects of drug candidates. The methods set forth herein allow for the evaluation of the biological effects of JNK inhibitors and, accordingly, are useful in a clinical setting, such as by providing a straight-forward avenue for following the in vivo activity of a JNK inhibitor, and for assessing the sensitivity of a particular patient population to treatment with JNK inhibitors, in particular oral JNK inhibitors. Citation or identification of any reference in Section 2 of this application is not to be construed as an admission that the reference is prior art to the present application. Part 3. SUMMARY: Provided herein are methods for evaluating the effect of 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof (“Compound 1”) in a patient, comprising UVB-irradiation of a patient's skin, administration of Compound 1, and measurement of phosphorylated c-Jun expression in skin using immunohistochemistry. In some embodiments, Compound 1 is administered orally. Also provided herein are methods for evaluating the effect of 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof (“Compound 1”) in a patient, comprising 1) measuring phosphorylated c-Jun expression in a first skin sample obtained from a first portion of a patient's skin irradiated with UVB-irradiation, 2) measuring phosphorylated c-Jun expression in a second skin sample obtained from a second portion of a patient's skin irradiated with UVB-irradiation after the patient has been administered Compound 1, and 3) comparing the levels of phosphorylated c-Jun in said first skin sample and said second skin sample. The measurement may be carried out in the skin samples using immunohistochemistry. The UVB irradiation may be at 2× minimum erythema dose (MED). The skin in the second skin sample may have been irradiated with UVB irradiation about 2 hours after administration of 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof. The skin sample may have been obtained from the portion of skin irradiated with UVB irradiation on the patient's buttock. The second skin sample may have been obtained about 8 hours after the exposure of the skin to UVB irradiation. The measurement of the amount of phosphorylated c-Jun in a skin sample can comprise an immunohistochemical analysis wherein a primary antibody is directed against the phosphorylated c-Jun to form an antibody/phosphorylated c-Jun complex and incubation with a secondary antibody conjugated with a chromogenic enzyme provides a color deposit marking the location of the primary antibody/phoshorylated c-Jun complex in the skin sample. The measurement may further comprise subjective scoring of the color marking or quantitative analysis using a laser scanning cytometer. Compound 1 may be administered orally. In one embodiment, provided herein are methods for identifying a patient (or patient population) who is sensitive to Compound 1, comprising exposing a first portion of said patient's skin to UVB irradiation, obtaining a sample of said first portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said first portion of said patient's skin, administering an effective amount of Compound 1 to said patient, exposing a second portion of said patient's skin to UVB irradiation, obtaining a sample of said second portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said second portion of said patient's skin, and comparing the levels of phosphorylated c-Jun in said first portion of said patient's skin and said second portion of said patient's skin, wherein the decrease in the level of phosphorylated c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin indicates that said patient is sensitive to Compound 1. Also provided herein are methods for identifying a patient (or patient population) who is sensitive to Compound 1, comprising: 1) measuring the amount of phosphorylated c-Jun in a first skin sample obtained from a first portion of a patient's skin irradiated with UVB irradiation, 2) measuring the amount of phosphorylated c-Jun in a second skin sample obtained from a second portion of a patient's skin irradiated with UVB irradiation after said patient has been administered Compound 1, and 3) comparing the levels of phosphorylated c-Jun in said first skin sample and said second skin sample, wherein a decrease in the level of phosphorylated c-Jun in said second skin sample to said first skin sample indicates that said patient is sensitive to Compound 1. The decrease in the level can be at least about 5%, about 10%, about 15%, about 20%, about 25%, about 30%, about 35%, about 40%, about 45%, about 50% or more. In another embodiment, provided herein are methods for evaluating the effect of Compound 1 in a patient, comprising UVB-irradiation of a patient's skin, administration of Compound 1, and measurement of phosphorylated c-Jun expression in skin using immunohistochemistry. Also provided herein are methods for evaluating the effect of Compound 1 in a patient, wherein the method comprises measuring phosphorylated c-Jun expression using immunohistochemistry in skin samples irradiated with UVB irradiation after the patient has been administered Compound 1. In another embodiment, provided herein are methods for evaluating inhibition of JNK in a patient by measuring phosphorylated c-Jun in the patient's skin. In one embodiment, provided herein are methods of measuring inhibition of JNK in a patient by exposing a first portion of said patient's skin to UVB irradiation, obtaining a sample of said first portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said first portion of said patient's skin, administering Compound 1 to said patient, exposing a second portion of said patient's skin to UVB irradiation, obtaining a sample of said second portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said second portion of said patient's skin, and comparing the levels of phosphorylated c-Jun in said first portion of said patient's skin and said second portion of said patient's skin, wherein a decreased level of phosphorylated c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin indicates inhibition of JNK. In another embodiment, methods for determining a dose-response relationship for the administration of Compound 1 in a patient are provided. The methods comprise administering to said patient varying doses (e.g., from about 1 mg to 1000 mg) of Compound 1 and determining the amount of JNK inhibition in said patient resulting from each dose of Compound 1, comprising exposing a first portion of said patient's skin to UVB irradiation, obtaining a sample of said first portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said first portion of said patient's skin, administering a dose of Compound 1 to said patient, exposing a second portion of said patient's skin to UVB irradiation, obtaining a sample of said second portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said second portion of said patient's skin, and comparing the levels of phosphorylated c-Jun in said first portion of said patient's skin and said second portion of said patient's skin, wherein the decrease in the level of phosphorylated c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin is proportional to the inhibition of JNK. Also provided herein is a method for determining a dose-response relationship for the administration of Compound 1, comprising: 1) measuring the amount of phosphorylated c-Jun in a first skin sample obtained from a first portion of a patient's skin irradiated with UVB irradiation, 2) measuring the amount of phosphorylated c-Jun in a second skin sample obtained from a second portion of a patient's skin irradiated with UVB irradiation after said patient has been administered varying doses of Compound 1 (e.g., from about 1 mg to 1000 mg), and 3) comparing the levels of phosphorylated c-Jun in said first skin sample and said second skin sample, wherein a decrease in the level of phosphorylated c-Jun in said second skin sample to said first skin sample is proportional to the inhibition of JNK. The decrease in the level may be at least about 5%, about 10%, about 15%, about 20%, about 25%, about 30%, about 35%, about 40%, about 45%, about 50% or more. In other embodiments, methods for determining the effective amount of Compound 1 for the treatment or management of a disease or condition associated with JNK in a patient are provided, which comprise administering to said patient varying doses (e.g., from about 1 mg to 1000 mg) of Compound 1 and determining the amount of JNK inhibition in said patient resulting from each dose of Compound 1, comprising exposing a first portion of said patient's skin to UVB irradiation, obtaining a sample of said first portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said first portion of said patient's skin, administering a dose of Compound 1 to said patient, exposing a second portion of said patient's skin to UVB irradiation, obtaining a sample of said second portion of said patient's skin, measuring the amount of phosphorylated c-Jun in said second portion of said patient's skin, and comparing the levels of phosphorylated c-Jun in said first portion of said patient's skin and said second portion of said patient's skin, wherein a 50% decrease in the level of phosphorylated c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin is indicative of the administration of an effective amount of Compound 1. Also provided herein is a method for determining an effective amount of Compound 1, comprising: 1) measuring the amount of phosphorylated c-Jun in a first skin sample obtained from a first portion of a patient's skin irradiated with UVB irradiation, 2) measuring the amount of phosphorylated c-Jun in a second skin sample obtained from a second portion of a patient's skin irradiated with UVB irradiation after said patient has been administered varying doses of Compound 1 (e.g., from about 1 mg to 1000 mg), and 3) comparing the levels of phosphorylated c-Jun in said first skin sample and said second skin sample, wherein a 50% decrease in the level of phosphorylated c-Jun in said second skin sample to said first skin sample is indicative of the administration of an effective amount of Compound 1. In yet another embodiment, a method for monitoring patient compliance with Compound 1 therapy is provided. The method comprises measuring the level of phosphorylated c-Jun or c-Jun expressed in a sample of the patient's skin and determining if the expression level is increased or decreased in the sample of the patient's skin compared to the expression level in a control untreated sample, wherein decreased expression indicates patient compliance with the Compound 1 therapy. The JNK inhibitor useful in the methods provided herein is: having the alternative names 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or 2-[(1,1-dimethylethyl)amino]-4-[[(1R,3R,4R)-3-hydroxy-4-methylcyclohexyl]amino]-5-pyrimidinecarboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof (collectively referred to herein as “Compound 1”). Compound 1 is disclosed in U.S. Patent Application Publication No. 2013/0029987, published on Jan. 31, 2013, and International Pub. No. WO2012/145569, the entireties of each of which are incorporated by reference herein. Part 5. DETAILED DESCRIPTION: Part 5.1. Definitions: The term “JNK” means a protein or an isoform thereof expressed by a JNK 1, JNK 2, or JNK 3 gene (Gupta, S., Barrett, T., Whitmarsh, A. J., Cavanagh, J., Sluss, H. K., Derijard, B. and Davis, R. J. The EMBO J. 15:2760-2770 (1996)). As used herein, the term “pharmaceutically acceptable salt(s)” refers to a salt prepared from a pharmaceutically acceptable non-toxic acid or base including an inorganic acid and base and an organic acid and base. Suitable pharmaceutically acceptable base addition salts of the compounds of formula (I) include, but are not limited to metallic salts made from aluminum, calcium, lithium, magnesium, potassium, sodium and zinc or organic salts made from lysine, N,N′-dibenzylethylenediamine, chloroprocaine, choline, diethanolamine, ethylenediamine, meglumine (N-methyl-glucamine) and procaine. Suitable non-toxic acids include, but are not limited to, inorganic and organic acids such as acetic, alginic, anthranilic, L-asparate, benzenesulfonic, benzoic, camphorsulfonic, citric, ethenesulfonic, formic, fumaric, furoic, galacturonic, gluconic, glucuronic, glutamic, glycolic, hydrobromic, hydrochloric, isethionic, lactic, maleic, malic, mandelic, methanesulfonic, mucic, nitric, pamoic, pantothenic, phenylacetic, phosphoric, propionic, salicylic, stearic, succinic, sulfanilic, sulfuric, tartaric acid, and p-toluenesulfonic acid. Specific non-toxic acids include hydrochloric, hydrobromic, maleic, phosphoric, sulfuric, and methanesulfonic acids. Examples of specific salts thus include hydrochloride and mesylate salts. Others are well-known in the art, see for example, Remington's Pharmaceutical Sciences, 18th eds., Mack Publishing, Easton Pa. (1990) or Remington: The Science and Practice of Pharmacy, 19th eds., Mack Publishing, Easton Pa. (1995). As used herein and unless otherwise indicated, the term “stereoisomer” or “stereomerically pure” means one stereoisomer of a compound of formula (I) that is substantially free of other stereoisomers of that compound. For example, a stereomerically pure compound having one chiral center will be substantially free of the opposite enantiomer of the compound. A stereomerically pure compound having two chiral centers will be substantially free of other diastereomers of the compound. A typical stereomerically pure compound comprises greater than about 80% by weight of one stereoisomer of the compound and less than about 20% by weight of other stereoisomers of the compound, greater than about 90% by weight of one stereoisomer of the compound and less than about 10% by weight of the other stereoisomers of the compound, greater than about 95% by weight of one stereoisomer of the compound and less than about 5% by weight of the other stereoisomers of the compound, or greater than about 97% by weight of one stereoisomer of the compound and less than about 3% by weight of the other stereoisomers of the compound. The compounds of formula (I) can have chiral centers and can occur as racemates, individual enantiomers or diastereomers, and mixtures thereof. All such isomeric forms are included within the embodiments disclosed herein, including mixtures thereof. The use of stereomerically pure forms of such compounds of formula (I), as well as the use of mixtures of those forms, are encompassed by the embodiments disclosed herein. For example, mixtures comprising equal or unequal amounts of the enantiomers of a particular compound of formula (I) may be used in methods and compositions disclosed herein. These isomers may be asymmetrically synthesized or resolved using standard techniques such as chiral columns or chiral resolving agents. See, e.g., Jacques, J., et al., Enantiomers, Racemates and Resolutions (Wiley-Interscience, New York, 1981); Wilen, S. H., et al., Tetrahedron 33:2725 (1977); Eliel, E. L., Stereochemistry of Carbon Compounds (McGraw-Hill, NY, 1962); and Wilen, S. H., Tables of Resolving Agents and Optical Resolutions p. 268 (E. L. Eliel, Ed., Univ. of Notre Dame Press, Notre Dame, Ind., 1972). It should also be noted the compounds of formula (I) can include E and Z isomers, or a mixture thereof, and cis and trans isomers or a mixture thereof. In certain embodiments, the compounds of formula (I) are isolated as either the E or Z isomer. In other embodiments, the compounds of formula (I) are a mixture of the E and Z isomers. The term “tautomers” refers to isomeric forms of a compound that are in equilibrium with each other. The concentrations of the isomeric forms will depend on the environment the compound is found in and may be different depending upon, for example, whether the compound is a solid or is in an organic or aqueous solution. For example, in aqueous solution, pyrazoles may exhibit the following isomeric forms, which are referred to as tautomers of each other: Compound 1 contains one or more chiral centers, and can exist as racemic mixtures of enantiomers, mixtures of diastereomers or enantiomerically or optically pure compounds. The use of stereomerically pure forms of such compounds, as well as the use of mixtures of those forms are encompassed by the embodiments disclosed herein. As a non-limiting example, mixtures comprising equal or unequal amounts of the enantiomers of Compound 1 may be used in methods and compositions disclosed herein. These isomers may be asymmetrically synthesized or resolved using standard techniques such as chiral columns or chiral resolving agents. See, e.g., Jacques, J., et al., Enantiomers, Racemates and Resolutions (Wiley-Interscience, New York, 1981); Wilen, S. H., et al., Tetrahedron 33:2725 (1977); Eliel, E. L., Stereochemistry of Carbon Compounds (McGraw-Hill, NY, 1962); and Wilen, S. H., Tables of Resolving Agents and Optical Resolutions p. 268 (E. L. Eliel, Ed., Univ. of Notre Dame Press, Notre Dame, Ind., 1972). The term “treating” as used herein, means an alleviation, in whole or in part, of a disorder, disease or condition, or one or more of the symptoms associated with a disorder, disease, or condition, or slowing or halting of further progression or worsening of those symptoms, or alleviating or eradicating the cause(s) of the disorder, disease, or condition itself. In one embodiment, the disorder is a liver fibrotic disorder, such as non-alcoholic steatohepatitis, steatosis (i.e. fatty liver), cirrhosis, primary sclerosing cholangitis, primary biliary cirrhosis, hepatitis, hepatocellular carcinoma, or liver fibrosis coincident with chronic or repeated alcohol ingestion (alcoholic hepatitis), with infection (e.g. viral infection such as HCV), with liver transplant, or with drug induced liver injury (e.g. acetaminophen toxicity). In some embodiments, “treating” means an alleviation, in whole or in part, of a disorder, disease or condition, or symptoms associated with diabetes or metabolic syndrome leading to liver fibrotic disorders, such as non-alcoholic steatohepatitis, steatosis (i.e. fatty liver), hepatitis or cirrhosis, or a slowing, or halting of further progression or worsening of those symptoms. In one embodiment, the symptom is jaundice. In another embodiment, “treating” means and alleviation, in whole or in part, of a disorder, disease or condition, or symptoms associated with a condition, treatable or preventable by inhibition of a JNK pathway. The term “preventing” as used herein, means a method of delaying and/or precluding the onset, recurrence or spread, in whole or in part, of a disorder, disease or condition; barring a subject from acquiring a disorder, disease, or condition; or reducing a subject's risk of acquiring a disorder, disease, or condition. In one embodiment, the disorder is a liver fibrotic disorder, or diabetes or metabolic syndrome leading to liver fibrotic disorders, as described herein, or symptoms thereof. In one embodiment, the disorder is a liver fibrotic disorder, such as non-alcoholic steatohepatitis, steatosis (i.e. fatty liver), cirrhosis, primary sclerosing cholangitis, primary biliary cirrhosis, hepatitis, hepatocellular carcinoma, or liver fibrosis coincident with chronic or repeated alcohol ingestion (alcoholic hepatitis), with infection (e.g. viral infection such as HCV), with liver transplant, or with drug induced liver injury (e.g. acetaminophen toxicity). In another, the disorder is a condition, treatable or preventable by inhibition of a JNK pathway. The terms “sensitivity” and “sensitive” when made in reference to treatment is a relative term which refers to the degree of effectiveness of Compound 1 in lessening or decreasing the symptoms of the disease being treated. For example, the term “increased sensitivity” when used in reference to treatment of a cell or patient refers to an increase of, at least a 5%, or more, in the effectiveness in lessening or decreasing the symptoms of a disease or condition associated with JNK when measured using any methods well-accepted in the art or as disclosed herein. The term “effective amount” in connection with Compound 1 means an amount capable of treating or preventing a disorder, disease or condition, or symptoms thereof, disclosed herein. As used herein “UVB” refers to electro-magnetic radiation that is in the region of the ultraviolet spectrum which extends from about 280 nm to about 320 nm. The term “likelihood” generally refers to an increase in the probability of an event. The term “likelihood” when used in reference to the effectiveness of a patient response generally contemplates an increased probability that the symptoms of a disease or condition associated with JNK will be lessened or decreased. The term “predict” generally means to determine or tell in advance. When used to “predict” the effectiveness of Compound 1 treatment, for example, the term “predict” can mean that the likelihood of the outcome of the treatment can be determined at the outset, before the treatment has begun, or before the treatment period has progressed substantially. The term “monitor,” as used herein, generally refers to the overseeing, supervision, regulation, watching, tracking, or surveillance of an activity. For example, the term “monitoring the efficacy of a treatment for a disease or condition associated with JNK” refers to tracking the effectiveness in treating a patient. Similarly, the term “monitoring,” when used in connection with patient compliance, either individually, or in a clinical trial, refers to the tracking or confirming that the patient is actually following the treatment regimen being tested as prescribed. The terms “determining”, “measuring”, “evaluating”, “assessing” and “assaying” as used herein generally refer to any form of measurement, and include determining if an element is present or not. These terms include both quantitative and/or qualitative determinations. Assessing may be relative or absolute. “Assessing the presence of” can include determining the amount of something present, as well as determining whether it is present or absent. “Patient” or “subject” is defined herein to include animals, such as mammals, including, but not limited to, primates (e.g., humans), cows, sheep, goats, horses, dogs, cats, rabbits, rats, mice, monkeys, chickens, turkeys, quails, or guinea pigs and the like, in one embodiment a mammal, in another embodiment a human. In one embodiment, a subject is a human having or at risk for having interstitial pulmonary fibrosis, systemic sclerosis, scleroderma, chronic allograft nephropathy, antibody mediated rejection, or lupus. In another, a subject is a human having or at risk for having liver fibrotic disorders or diabetes or metabolic syndrome leading to liver fibrotic disorders, or a condition, treatable or preventable by inhibition of a JNK pathway, or a symptom thereof. In one embodiment, a subject is fasted. In another embodiment, a subject is fed. Part 5.2. Use of c-Jun N-Terminal Kinases as Biomarkers: Methods provided herein are based, in part, on the discovery that the presence and level of phosphorylated c-Jun or c-Jun in patient skin samples can be utilized as a biomarker to follow the inhibition of JNK. In particular, these biomarkers can be used to predict, assess, and track the effectiveness of Compound 1 therapy in a patient, in particular oral therapy with Compound 1, or to monitor the patient's compliance to the prescribed regimen of Compound 1 therapy. The baseline phosphorylated c-Jun immune-reactivity in healthy human skin is low without UVB exposure. UVB-irradiation reliably increases levels of phosphorylated c-Jun, as reflected by an increase in phosphorylated c-Jun immunoreactivity in tissue sections. The increase starts to plateau at approximately 8 hours post UVB exposure. The inhibition of JNK is dose-related. UVB-irradiation induced increases in phosphorylated c-Jun can be used as a model to evaluate Compound 1, including the evaluation of dose-response, and to identify patient populations who are sensitive to Compound 1. Provided herein are methods relating to the use of phosphorylated c-Jun levels induced by UVB-irradiation as a biomarker to evaluate the effectiveness of Compound 1. Phosphorylated c-Jun and c-Jun levels can be used to determine whether a treatment is likely to be successful in diseases or conditions associated with JNK. In certain embodiments, the methods provided herein allow for the amount of in vivo inhibition of JNK resulting from administration of Compound 1 to be determined. In certain embodiments, the assays provided herein comprise exposing a first portion of said patient's skin to UVB irradiation, obtaining a sample of said first portion of said patient's skin, measuring the amount of phosphorylated c-Jun or c-Jun in said first portion of said patient's skin immunohistochemically, administering Compound 1 to said patient, exposing a second portion of said patient's skin to UVB irradiation, obtaining a sample of said second portion of said patient's skin, measuring the amount of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin immunohistochemically, and comparing the levels of phosphorylated c-Jun or c-Jun in said first portion of said patient's skin and said second portion of said patient's skin, wherein a reduction of levels of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin compared to said first portion of said patient's skin indicates inhibition of JNK. Also provided herein is a method for evaluating inhibition of JNK in a patient comprising: 1) measuring the amount of phosphorylated c-Jun or c-Jun in a first skin sample obtained from a first portion of a patient's skin irradiated with UVB irradiation, 2) measuring the amount of phosphorylated c-Jun or c-Jun in a second skin sample obtained from a second portion of a patient's skin irradiated with UVB irradiation after said patient has been administered Compound 1, and 3) comparing the levels of phosphorylated c-Jun in said first skin sample and said second skin sample, wherein a reduction of levels of phosphorylated c-Jun or c-Jun in said second skin sample to said first skin sample indicates inhibition of JNK. In some embodiments the reduction is at least about 5%, about 10%, about 15%, about 20%, about 25%, about 30%, about 35%, about 40%, about 45%, about 50% or more. In certain embodiments, the assays provided herein comprise using human skin model tissues. In such embodiments, the assays comprise exposing a first sample of said tissue to UVB irradiation, obtaining a sample of said first portion of said tissue, measuring the amount of phosphorylated c-Jun or c-Jun in said first portion of said tissue immunohistochemically, administering Compound 1 to said tissue, exposing a second portion of said tissue to UVB irradiation, obtaining a sample of said second portion of said tissue, measuring the amount of phosphorylated c-Jun or c-Jun in said second portion of said tissue immunohistochemically, and comparing the levels of phosphorylated c-Jun or c-Jun in said first portion of said tissue and said second portion of said tissue, wherein a reduction of levels of phosphorylated c-Jun or c-Jun in said second portion of said tissue compared to said first portion of said tissue indicates inhibition of JNK. In some embodiments the reduction is at least about 5%, about 10%, about 15%, about 20%, about 25%, about 30%, about 35%, about 40%, about 45%, about 50% or more. In such embodiments, human skin model tissues such as EpiDermFT may be used. EpiDermFT is a reconstituted human skin equivalent, which exhibits morphological and growth characteristics similar to human skin, and has been used widely as a model tissue system in studies relevant to human skin (see, e.g., Zhao J F, Zhang Y J, Kubilus J, Jin X H, Santella R M, Athar M, Wang Z Y, Bickers D R. Reconstituted 3-Dimensional Human Skin as a Novel in Vitro Model for Studies of Carcinogen, Biochemical and Biophysical Research Comms. 1999; 254:49-53; Mahns A, Wolber R, Stab F, Klotz L O, Sies H, Contribution of UVB and UVA to UV-dependent stimulation of cyclooxygenase-2 expression in articfical epidermis, Photochem. Photobiol. Sci. 2004; 3:257-62; Sedelnikova O A, Nakamura A, Kovalchuk O, Koturbash I, Mitchell S A, Marino S A, Brenner D J, Bonner W M, DNA Double-Strand Breaks Form in Bystander Cells after Microbeam Irradiation of Three-dimensional Human Tissue Models, Cancer Res 2007; 67(9):4295-4302; Hayden P J, Burnham B, Klausner M, Kubilus J, Sheasgreen J E, Wound Healing Response of the EpiDerm Full Thickness (EpiDerm-FT) In Vitro Human Skin Equivalent after Solar UV Irradiation, Presented at the 5th World Congress, Berlin, Germany, August 2005 & The Society of Investigative Dermatology Meeting, Providence, R.I., April-May 2004, TR-328:1-10). EpiDermFT samples may be obtained from MatTek Corporation (Ashland, Mass.). In some embodiments, the immunohistochemistry evaluations of the skin biopsies provided by the methods herein to assess JNK activation comprise a two antibody IHC assay that employs a primary antibody, directed against the target phosphorylated c-Jun or c-Jun, and a secondary antibody conjugated with a chromogenic enzyme. In such embodiments, the secondary antibody-reporter conjugate deposits a red color when incubated with the substrate reaction mixture, thus marking the location of the primary antibody target complex. This red color is then recorded with standard bright-field illumination using, e.g., a Nikon microscope. The microscope images are then photographed and electronic images may be scored (blinded) by independent and trained scorers using guidelines as illustrated in the Examples. In certain embodiments, exploratory quantitative IHC analysis may be carried out using a laser scanning cytometer. In such embodiments, the slides are further processed in order to define the nuclear compartment of the epithelial keratinocytes. In such embodiments, the same IHC slides are counterstained with Hematoxylin to tag the nuclear compartment, then scanned using two photodiode channels, 488 nm for the DAB stain (to mark the primary antibody directed against phosphorylated c-Jun or c-Jun) and 633 nm for the Hematoxylin stain, then the nuclei are counted based upon the Hematoxylin signal and then the DAB signals are integrated for each nucleus in the epithelium. In some embodiments, the methods provided herein allow for the measurement of phosphorylated c-Jun or c-Jun levels, before and after administration of Compound 1, which can be used as biomarkers for measuring the inhibition of JNK by Compound 1 in a patient. In some embodiments of the methods provided herein, a decreased level of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin indicates inhibition of JNK by Compound 1. In some embodiments of the methods provided herein, a decreased level of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin is proportional to the inhibition of JNK by Compound 1. In some embodiments, the methods provided herein allow for the measurement of phosphorylated c-Jun or c-Jun levels before and after administration of Compound 1, which can be used as biomarkers for determining whether a patient is sensitive to Compound 1. In some embodiments of the methods provided herein, a decreased level of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin indicates that said patient is sensitive to Compound 1. In some embodiments, the methods provided herein allow for the measurement of phosphorylated c-Jun or c-Jun levels before and after administration of Compound 1, which can be used to determine the effective amount of Compound 1 for the treatment or prevention of a disease or condition associated with JNK in a patient. In some embodiments of the methods provided herein, a decreased level of phosphorylated c-Jun or c-Jun in said second portion of said patient's skin relative to said first portion of said patient's skin may be correlated to indicate the administration of an effective amount of Compound 1. Part 5.3. Compound 1: The JNK inhibitor useful in the methods provided herein is: having the alternative names 2-(tert-butylamino)-4-((1R,3R,4R)-3-hydroxy-4-methylcyclohexylamino)-pyrimidine-5-carboxamide or 2-[(1,1-dimethylethyl)amino]-4-[[(1R,3R,4R)-3-hydroxy-4-methylcyclohexyl]amino]-5-pyrimidinecarboxamide or a pharmaceutically acceptable stereoisomer, tautomer, solid form, polymorph, salt, hydrate, clathrate, or solvate thereof (“collectively referred to herein as “Compound 1”). Compound 1 is disclosed in U.S. Patent Application Publication No. 2013/0029987, published on Jan. 31, 2013, and International Pub. No. WO2012/145569, the entireties of each of which are incorporated by reference herein. In one embodiment, Compound 1 is a free base. In certain embodiments, the free base is a solid. In certain embodiments, the free base is an amorphous solid. In yet another embodiment, the free base is crystalline. In another embodiment, Compound 1 is a pharmaceutically acceptable solvate of the free base. In one embodiment, the solvate is a hydrate. In another embodiment, the hydrate is in a crystalline form. It should be noted that if there is a discrepancy between a depicted structure and a name given that structure, the depicted structure is to be accorded more weight. In addition, if the stereochemistry of a structure or a portion of a structure is not indicated with, for example, bold or dashed lines, the structure or portion of the structure is to be interpreted as encompassing all stereoisomers of it. Part 5.4. Methods for Making Compound 1: Compound 1 can be made using conventional organic syntheses using reagents and methods known in the art, including the methods provided in U.S. Patent Application Publication No. 2013/0029987, published on Jan. 31, 2013, U.S. Provisional Patent Application No. 61/933,636, filed on Jan. 30, 2014, U.S. Provisional Patent Application No. 62/025,161, filed on Jul. 16, 2014, and International Pub. No. WO2012/145569, the entire contents of each of which are incorporated herein by reference. Part 5.5. Methods of Administration and Dosage: Compound 1 can be administered to a subject orally, topically or parenterally in the conventional form of preparations, such as capsules, microcapsules, tablets, granules, powder, troches, pills, suppositories, injections, suspensions, syrups, patches, creams, lotions, ointments, gels, sprays, solutions and emulsions. Suitable formulations can be prepared by methods commonly employed using conventional, organic or inorganic additives, such as an excipient (e.g., sucrose, starch, mannitol, sorbitol, lactose, glucose, cellulose, talc, calcium phosphate or calcium carbonate), a binder (e.g., cellulose, methylcellulose, hydroxymethylcellulose, polypropylpyrrolidone, polyvinylpyrrolidone, gelatin, gum arabic, polyethyleneglycol, sucrose or starch), a disintegrator (e.g., starch, carboxymethylcellulose, hydroxypropylstarch, low substituted hydroxypropylcellulose, sodium bicarbonate, calcium phosphate or calcium citrate), a lubricant (e.g., magnesium stearate, light anhydrous silicic acid, talc or sodium lauryl sulfate), a flavoring agent (e.g., citric acid, menthol, glycine or orange powder), a preservative (e.g, sodium benzoate, sodium bisulfite, methylparaben or propylparaben), a stabilizer (e.g., citric acid, sodium citrate or acetic acid), a suspending agent (e.g., methylcellulose, polyvinyl pyrroliclone or aluminum stearate), a dispersing agent (e.g., hydroxypropylmethylcellulose), a diluent (e.g., water), and base wax (e.g., cocoa butter, white petrolatum or polyethylene glycol). The effective amount of Compound 1 in the pharmaceutical composition may be at a level that will exercise the desired effect; for example, about 0.005 mg/kg of a subject's body weight to about 10 mg/kg of a subject's body weight in unit dosage for both oral and parenteral administration. The dose of Compound 1 to be administered to a subject is rather widely variable and can be subject to the judgment of a health-care practitioner. In general, Compound 1 can be administered one to four times a day in a dose of about 0.005 mg/kg of a subject's body weight to about 10 mg/kg of a subject's body weight in a subject, but the above dosage may be properly varied depending on the age, body weight and medical condition of the subject and the type of administration. In one embodiment, the dose is about 0.01 mg/kg of a subject's body weight to about 5 mg/kg of a subject's body weight, about 0.05 mg/kg of a subject's body weight to about 1 mg/kg of a subject's body weight, about 0.1 mg/kg of a subject's body weight to about 0.75 mg/kg of a subject's body weight or about 0.25 mg/kg of a subject's body weight to about 0.5 mg/kg of a subject's body weight. In one embodiment, one dose is given per day. In any given case, the amount of Compound 1 administered will depend on such factors as the solubility of the active component, the formulation used and the route of administration. In one embodiment, application of a topical concentration provides intracellular exposures or concentrations of about 0.01-10 μM. In another embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 0.375 mg/day to about 750 mg/day, about 0.75 mg/day to about 375 mg/day, about 3.75 mg/day to about 75 mg/day, about 7.5 mg/day to about 55 mg/day or about 18 mg/day to about 37 mg/day of Compound 1 to a subject in need thereof. In another embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 1 mg/day to about 1200 mg/day, about 10 mg/day to about 1200 mg/day, about 100 mg/day to about 1200 mg/day, about 400 mg/day to about 1200 mg/day, about 600 mg/day to about 1200 mg/day, about 400 mg/day to about 800 mg/day, about 60 mg/day to about 720 mg/day, about 240 mg/day to about 720 mg/day or about 600 mg/day to about 800 mg/day of Compound 1 to a subject in need thereof. In another embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of Compound 1. In yet another embodiment, provided herein are methods for the treatment and prevention of a disease or disorder comprising administration of about 10 mg/day, about 30 mg/day, about 60 mg/day, about 120 mg/day, about 160 mg/day, about 200 mg/day, about 240 mg/day, about 400 mg/day, about 480 mg/day, or about 720 mg/day per day of Compound 1. In a particular embodiment, the methods disclosed herein comprise the administration of about 400 mg/day, about 600 mg/day or about 800 mg/day of Compound 1 to a subject in need thereof. In a particular embodiment, the methods disclosed herein comprise the administration of about 60 mg/day, about 160 mg/day or about 400 mg/day of Compound 1 to a subject in need thereof. In another embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 10 mg/day to about 720 mg/day, about 10 mg/day to about 480 mg/day, about 60 mg/day to about 720 mg/day or about 240 mg/day to about 720 mg/day of Compound 1 to a subject in need thereof. In one embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 10 mg/day, about 30 mg/day, about 60 mg/day, about 120 mg/day, about 240 mg/day, about 480 mg/day, or about 720 mg/day of Compound 1 to a subject in need thereof. In one embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 60 mg/day, about 160 mg/day, or about 400 mg/day of Compound 1 to a subject in need thereof. In another embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration about 200 mg/day of Compound 1 to a subject in need thereof. In one embodiment, provided herein are methods for the treatment or prevention of a disease or disorder comprising the administration of about 10 mg/day, about 30 mg/day, about 60 mg/day, about 120 mg/day, about 160 mg/day, about 200 mg/day, about 240 mg/day, about 400 mg/day, about 480 mg/day, or about 720 mg/day of Compound 1 to a subject in need thereof. In another embodiment, provided herein are unit dosage formulations that comprise between about 10 mg and about 100 mg, about 1 mg and about 200 mg, about 30 mg and about 200 mg, about 35 mg and about 1400 mg, about 125 mg and about 1000 mg, about 250 mg and about 1000 mg, or about 500 mg and about 1000 mg of Compound 1. In another embodiment, provided herein are unit dosage formulations that comprise about 1 mg, about 5 mg, about 10 mg, about 15 mg, about 20 mg, about 30 mg, about 35 mg, about 50 mg, about 60 mg, about 70 mg, about 100 mg, about 120 mg, about 125 mg, about 140 mg, about 175 mg, about 200 mg, about 240 mg, about 250 mg, about 280 mg, about 350 mg, about 480 mg, about 500 mg, about 560 mg, about 700 mg, about 720 mg, about 750 mg, about 1000 mg or about 1400 mg of Compound 1. In another embodiment, provided herein are unit dosage forms that comprise about 30 mg, about 100 mg or about 200 mg of Compound 1. Pharmaceutical compositions, and dosage forms of Compound 1 can be administered once, twice, three, four or more times daily. In one embodiment, pharmaceutical compositions, and dosage forms of Compound 1 can be administered once daily for 14 days. Compound 1 can be administered orally for reasons of convenience. In one embodiment, when administered orally, Compound A is administered with a meal and water. In another embodiment, Compound 1 (e.g., granules or dispersible tablets) is dispersed in water or juice (e.g., apple juice or orange juice) and administered orally as a suspension. Compound 1 can also be administered intradermally, intramuscularly, intraperitoneally, percutaneously, intravenously, subcutaneously, intranasally, epidurally, sublingually, intracerebrally, intravaginally, transdermally, rectally, mucosally, by inhalation, or topically to the ears, nose, eyes, or skin. The mode of administration is left to the discretion of the health-care practitioner, and can depend in-part upon the site of the medical condition. In one embodiment, provided herein are capsules containing Compound 1 without an additional carrier, excipient or vehicle. In another embodiment, provided herein are compositions comprising an effective amount of Compound 1 and a pharmaceutically acceptable carrier or vehicle, wherein a pharmaceutically acceptable carrier or vehicle can comprise an excipient, diluent, or a mixture thereof. In one embodiment, the composition is a pharmaceutical composition. The compositions can be in the form of tablets, chewable tablets, capsules, solutions, parenteral solutions, troches, suppositories and suspensions and the like. Compositions can be formulated to contain a daily dose, or a convenient fraction of a daily dose, in a dosage unit, which may be a single tablet or capsule or convenient volume of a liquid. In one embodiment, the solutions are prepared from water-soluble salts, such as the hydrochloride salt. In general, all of the compositions are prepared according to known methods in pharmaceutical chemistry. Capsules can be prepared by mixing Compound 1 with a suitable carrier or diluent and filling the proper amount of the mixture in capsules. The usual carriers and diluents include, but are not limited to, inert powdered substances such as starch of many different kinds, powdered cellulose, especially crystalline and microcrystalline cellulose, sugars such as fructose, mannitol and sucrose, grain flours and similar edible powders. Tablets can be prepared by direct compression, by wet granulation, or by dry granulation. Their formulations usually incorporate diluents, binders, lubricants and disintegrators as well as the compound. Typical diluents include, for example, various types of starch, lactose, mannitol, kaolin, calcium phosphate or sulfate, inorganic salts such as sodium chloride and powdered sugar. Powdered cellulose derivatives are also useful. Typical tablet binders are substances such as starch, gelatin and sugars such as lactose, fructose, glucose and the like. Natural and synthetic gums are also convenient, including acacia, alginates, methylcellulose, polyvinylpyrrolidine and the like. Polyethylene glycol, ethylcellulose and waxes can also serve as binders. A lubricant might be necessary in a tablet formulation to prevent the tablet and punches from sticking in the dye. The lubricant can be chosen from such slippery
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