Title of Invention: MATERIALS AND METHODS FOR TREATMENT OF SEVERE COMBINED IMMUNODEFICIENCY (SCID) OR OMENN SYNDROME Abstract: The present application provides materials and methods for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome, both ex vive and in vive. In addition, the present application provides materials and methods for editing to modulate the expression, function or activity of the Recombination Activating Gene 1 (RAG1) gene in a cell by genome editing. Detailed Description: RELATED APPLICATIONS This application claims the benefit of U.S. Provisional Application No. 62/290,277, filed Feb. 2, 2016; and U.S. Provisional Application No. 62/324,032, filed Apr. 18, 2016; the contents of each of which are incorporated herein by reference in their entirety. The present application provides materials and methods for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome, both ex vivo and in vivo. In addition, the present application provides materials and methods for genome editing to modulate the expression, function or activity of the Recombination Activating Gene 1 (RAG1) gene in a cell. INCORPORATION BY REFERENCE OF SEQUENCE LISTING This application contains a Sequence Listing in computer readable form (filename: CRIS012001WO_ST25; 13,301,918 bytes—ASCII text file; created Jan. 26, 2017), which is incorporated herein by reference in its entirety and forms part of the disclosure. BACKGROUND Severe combined immunodeficiency (SCID) is a monogenic disease that affects approximately 1.7/100,000 people in the United States, with about 40-100 new cases per year (J. Allergy Clin Immunol 2007; 120: 760-8). Mutations in more than 20 different genes have been identified as causing SCID, including, but not limited to, IL2RG, ADA, RAG1, RAG2, IL7R, JAK3, CDLRE1, and others. SCID causes disturbed development of functional T cells and B cells. Infants with SCID develop infections starting at approximately three months. The disease is almost universally fatal in the first two years. Existing treatment for SCID is hematopoietic stem cell transplant, which at best has a 5 year survival rate of 74% overall or greater than 90% for a matched sibling donor (N. Engl. J. Med. 214; 371: 434-46). Mutations in the Recombination Activating Gene 1 (RAG1) can result in a number of severe combined immunodeficiencies (SCID), which include increased vulnerability to infectious diseases and shortened life expectancy. The impaired number and function of B and T cells in these patients is attributed to the key role of RAG1 (and RAG2) in the V(D)J recombination process that leads to the generation of diversity and assembly of the immunoglobulin (Ig) and T cell receptor (TCR) genes, in B cells and T cells, respectively. Depending on the types of mutation(s), the symptoms can range from SCID to autoimmunity resulting from dysregulation of the B and T cells. RAG1 is the catalytic component of the RAG complex, a multiprotein complex that mediates the DNA cleavage phase during V(D)J recombination (McBlane, J. F. et al. Cell 83, 387-395 (1995)). V(D)J recombination allows formation of the extensive repertoire of antigen-specific receptors. V(D)J stands for Variability, Diversity and Joining, the segments in the genes encoding Ig and TCR proteins. V(D)J recombination adds both combinatorial and junctional diversity. The combinatorial assembly results in a diverse range of Ig and TCR genes in developing B and T cells through the rearrangement of different pairings of V (variable), in some cases D (diversity), and J (joining) gene segments into fusion genes. The RAG proteins are part of a system that ensures that DNA rearrangements take place at the correct locations relative to the V, D, and J gene segment coding regions. The sites of V(D)J recombination are determined by highly conserved recombination signal sequences (RSSs). The RSS includes one heptamer and one nonamer motif flanking either a 12- or 23-base pair spacer. The so-called “12/23 rule” promotes the efficient rearrangements that generally occur only between RSSs on the same chromosome with the heptamer and nonamer separated by differing spacer lengths (Eastman, Q. M., Leu, T. M. & Schatz, D. G. Nature 380, 85-88 (1996)). RAG1 mediates DNA binding to the recombination signal sequences (RSS) catalyzing the DNA cleavage activity through introduction of a double-strand break between the RSS and an adjacent coding segment. V(D)J recombination is essential for the development of lymphocytes. Junctional diversity further expands the repertoire through end processing of the segment ends at the borders of the V, D, and J elements. There are no mature lymphocytes without V(D)J recombination. Mutations in recombinase-activating genes 1 or 2 (RAG1/2) represent approximately 17% of all SCID cases due to this requirement for V(D)J rearrangement for functional B and T cell receptors. (Fischer, A. et al., “Severe combined immunodeficiencies and related disorders.” Nat Rev Dis Primers, vol. 1: 15061 (2015)). RAG1 mutations can result in alpha/beta T-cell lymphopenia with gamma/delta T-cell expansion, severe cytomegalovirus (CMV) infection, and autoimmunity (Niehues, T., Perez-Becker, R. & Schuetz, C. Clin Immunol 135, 183-192 (2010) and Kalman, L. et al. Genet Med 6, 16-26 (2004)). Mutations resulting in complete RAG deficiency (RAGD or RAGΔ) with no V(D)J (<1% recombination activity of wild type) is associated with classical SCID and absence of T and B cells. A range of phenotypes present with hypomorphic mutations resulting in >1% of wild type activity: RAGD with skin inflammation and αβT-cell expansion (classical Omenn Syndrome), RAGD with skin inflammation and without T-cell expansion (incomplete Omenn Syndrome), RAGD with γδ T-cell expansion and RAGD with granulomas, early onset autoimmunity, idiophatic CD4 lymphopenia and a phenotype resembling common variable immunodeficiency (Geier, C. B. et al. PLoS One 10, e0133220 (2015)). Omenn Syndrome has particular symptoms related to the limited amounts of recombination present and dysregulation of T and B cell functions. Symptoms are similar to graft-versus-host disease (GVHD), as the patients can have abnormal T cells with affinity for self-antigens. These auto reactive cells can target the patient resulting in symptoms similar to GVHD, including chronic inflammation of the skin, eosinophilia, failure to thrive, swollen lymph nodes, swollen spleen, diarrhea and enlarged liver. These patients have low immunoglobulin levels (except immunoglobulin E, which is elevated), low T cell levels (of low diversity), and no B cells. An additional disease, distinct from classic SCID and from Omenn Syndrome, is combined cellular and humoral deficiencies and multiple granulomas (Boissel, S. et al. Nucleic Acids Res 42, 2591-2601 (2014)). Allogeneic bone marrow (BM) transplantation is a curative treatment that displays a high survival rate when a HLA compatible donor is available. There are complications with morbidity and mortality directly related to conditioning chemotherapy and graft-versus-host disease, which are reduced in newer protocols. There is a much poorer prognosis when the donor is partially compatible. There are large numbers of patients for whom HLA-matched donors are unavailable, which is a major challenge. An autologous procedure based on genetic correction of hematopoietic stem and progenitor cells is a highly attractive option, particularly for these patients. Early gene therapy methods used autologous hematopoietic stem cells modified to express the therapeutic gene via γ-retroviral vectors. There is increased risk from this type of treatment, as the level of expression of RAG1 can be dangerous as it is a nuclease whose function is controlling genetic rearrangements. In addition, using viral insertion as a means of cDNA delivery carries the significant risks of insertional mutagenesis, as gamma retrovirus preferentially target transcribed regions. This is avoided by targeting the cDNA to a defined “safe harbor” using nucleases for site-specific editing or ideally directly correcting the gene in situ, enabling correct transcriptional control. Genome engineering refers to the strategies and techniques for the targeted, specific modification of the genetic information (genome) of living organisms. Genome engineering is a very active field of research because of the wide range of possible applications, particularly in the areas of human health; the correction of a gene carrying a harmful mutation, for example, or to explore the function of a gene. Early technologies developed to insert a transgene into a living cell were often limited by the random nature of the insertion of the new sequence into the genome. Random insertions into the genome may result in disrupting normal regulation of neighboring genes leading to severe unwanted effects. Furthermore, random integration technologies offer little reproducibility, as there is no guarantee that the sequence would be inserted at the same place in two different cells. Recent genome engineering strategies, such as ZFNs, TALENs, HEs and MegaTALs, enable a specific area of the DNA to be modified, thereby increasing the precision of the correction or insertion compared to early technologies. These newer platforms offer a much larger degree of reproducibility. Despite efforts from researchers and medical professionals worldwide who have been trying to address SCID and Omenn Syndrome, and despite the promise of genome engineering approaches, there still remains a critical need for developing safe and effective treatments for SCID and Omenn Syndrome. The present invention presents an approach to correct the genetic basis of SCID and Omenn Syndrome. By using genome engineering tools to create permanent changes to the genome that can correct the RAG1 gene and restore RAG1 protein activity with a single treatment, the resulting therapy should stop the disease progression completely. SUMMARY Provided herein are cellular, ex vivo and in vivo methods for creating permanent changes to the genome by deleting, inserting, correcting or modulating the expression of or function of one or more mutations or exons within or near the Recombination Activating Gene 1 (RAG1) gene or other DNA sequences that encode regulatory elements of the RAG1 gene or knocking in RAG1 cDNA or minigene into a safe harbor locus by genome editing and restoring RAG1 protein activity, which can be used to treat severe combined immunodeficiency (SCID) or Omenn Syndrome. Also provided are components, kits and compositions for performing such methods. Also provided are cells produced by them. Provided herein is a method for editing a RAG1 gene in a human cell by genome editing, the method comprising the step of introducing into the human cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or one or more double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene that results in at least one of a permanent insertion, deletion, correction, or modulation of expression or function of one or more mutations or exons within or near or affecting the expression or function of the RAG1 gene, or within or near a safe harbor locus that results in a permanent insertion of the RAG1 gene or minigene, and results in restoration of RAG1 protein activity. Also provided herein is a method for inserting a RAG1 gene in a human cell by genome editing, the method comprising the step of: introducing into the human cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near a safe harbor locus that results in a permanent insertion of the RAG1 gene or minigene, and results in restoration of RAG1 protein activity. In one aspect, provided herein is a method for editing the Recombination Activating Gene 1 (RAG1) gene in a human cell by genome editing comprising introducing into the cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene of the cell that results in permanent deletion, insertion, or correction of one or more mutations within or near the RAG1 gene, or within or near a safe harbor locus that results in permanent insertion of the RAG1 gene or minigene, and restoration of RAG1 protein activity. In another aspect, provided herein is an ex vivo method for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome comprising the steps of: i) creating a patient specific induced pluripotent stem cell (iPSC); ii) editing within or near the Recombination Activating Gene 1 (RAG1) gene of the iPSC or other DNA sequences that encode regulatory elements of the RAG1 gene of the iPSC or editing within or near a safe harbor locus of the iPSC; iii) differentiating the genome edited iPSC into a hematopoietic progenitor cell or a white blood cell; and iv) implanting the hematopoietic progenitor cell or white blood cell into the patient. As used herein, the term “hematopoietic progenitor cell” includes hematopoietic stem cells. In some embodiments, the step of creating a patient specific induced pluripotent stem cell (iPSC) comprises: a) isolating a somatic cell from the patient; and b) introducing a set of pluripotency-associated genes into the somatic cell to induce the cell to become a pluripotent stem cell. In some embodiments, the somatic cell is a fibroblast. In some embodiments, the set of pluripotency-associated genes is one or more of the genes selected from the group consisting of OCT4, SOX2, KLF4, Lin28, NANOG and cMYC. The step of editing within or near a RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene of the iPSC or editing within or near a safe harbor locus of the RAG1 gene of the iPSC or editing within or near a locus of the first exon of the RAG1 gene of the iPSC can comprise introducing into the iPSC one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene that results in a permanent insertion, correction, deletion, or modulation of expression or function of one or more mutations or exons within or near or affecting the expression or function of the RAG1 gene or within or near a safe harbor locus that results in a permanent insertion of the RAG1 gene resulting in restoration of RAG1 protein activity. The safe harbor locus can be selected from the group consisting of AAVS1 (PPP1R12C), ALB, Angptl3, ApoC3, ASGR2, CCR5, FIX (F9), G6PC, Gys2, HGD, Lp(a), Pcsk9, Serpinal, TF, and TTR. The safe harbor locus can be selected from the group consisting of: exon 1-2 of AAVS1 (PPP1R12C), exon 1-2 of ALB, exon 1-2 of Angptl3, exon 1-2 of ApoC3, exon 1-2 of ASGR2, exon 1-2 of CCR5, exon 1-2 of FIX (F9), exon 1-2 of G6PC, exon 1-2 of Gys2, exon 1-2 of HGD, exon 1-2 of Lp(a), exon 1-2 of Pcsk9, exon 1-2 of Serpinal, exon 1-2 of TF, and exon 1-2 of TTR. In some embodiments, the step of editing the Recombination Activating Gene 1 (RAG1) gene of the iPSC comprises introducing into the iPSC one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene that results in permanent deletion, insertion, or correction of one or more mutations within or near the RAG1 gene and restoration of RAG1 protein activity. In some embodiments, the step of differentiating the genome edited iPSC into a hematopoietic progenitor cell or a white blood cell comprises one or more of the following: treatment with a combination of small molecules or delivery of master transcription factors. In some embodiments, the step of implanting the hematopoietic progenitor cell or white blood cell into the patient comprises implanting the hematopoietic progenitor cell or white blood cell into the patient by transplantation, local injection, or systemic infusion, or combinations thereof. In another aspect, provided herein is an ex vivo method for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome comprising the steps of: i) isolating a white blood cell from the patient; ii) editing within or near the Recombination Activating Gene 1 (RAG1) gene or other DNA sequences that encode regulatory elements of the RAG1 gene of the white blood cell or editing within or near a safe harbor locus of the white blood cell; and iii) implanting the genome-edited white blood cell into the patient. In some embodiments, the step of isolating a white blood cell from the patient comprises: cell differential centrifugation, cell culturing, or combinations thereof. In some embodiments, the step of editing within or near the Recombination Activating Gene 1 (RAG1) gene of the white blood cell or other DNA sequences that encode regulatory elements of the RAG1 gene of the white blood cell or editing within or near a safe harbor locus of the white blood cell comprises introducing into the white blood cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene that results in permanent insertion, correction, deletion, or modulation of expression or function of one or more mutations or exons within or near or affecting the expression or function of the RAG1 gene or editing within or near a safe harbor locus that results in permanent deletion, insertion, or correction of one or more mutations within or near the RAG1 gene and restoration of RAG1 protein activity. The safe harbor locus can be selected from the group consisting of AAVS1 (PPP1R12C), ALB, Angptl3, ApoC3, ASGR2, CCR5, FIX (F9), G6PC, Gys2, HGD, Lp(a), Pcsk9, Serpinal, TF, and TTR. The safe harbor locus can be selected from the group consisting of: exon 1-2 of AAVS1 (PPP1R12C), exon 1-2 of ALB, exon 1-2 of Angptl3, exon 1-2 of ApoC3, exon 1-2 of ASGR2, exon 1-2 of CCR5, exon 1-2 of FIX (F9), exon 1-2 of G6PC, exon 1-2 of Gys2, exon 1-2 of HGD, exon 1-2 of Lp(a), exon 1-2 of Pcsk9, exon 1-2 of Serpinal, exon 1-2 of TF, and exon 1-2 of TTR. In some embodiments, the step of implanting the edited white blood cell into the patient comprises implanting the edited white blood cell into the patient by transplantation, local injection, or systemic infusion, or combinations thereof. In an aspect, provided herein is an ex vivo method for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome comprising the steps of i) isolating a mesenchymal stem cell from the patient; ii) editing within or near the Recombination Activating Gene 1 (RAG1) gene of the stem cell or other DNA sequences that encode regulatory elements of the RAG1 gene of the mesenchymal stem cell or editing within or near a safe harbor locus of the RAG1 gene of the mesenchymal stem cell; iii) differentiating the genome-edited stem cell into a hematopoietic progenitor cell or white blood cell; and iv) implanting the hematopoietic progenitor cell or white blood cell into the patient. In some embodiments, the stem cell is isolated from the patients bone marrow or peripheral blood. In some embodiments, the step of isolating a mesenchymal stem cell from the patient comprises: aspiration of bone marrow and isolation of mesenchymal cells by density centrifugation using Percoll™. In some embodiments, the step of editing within or near the Recombination Activating Gene 1 (RAG1) gene of the stem cell or other DNA sequences that encode regulatory elements of the RAG1 gene of the mesenchymal stem cell comprises introducing into the mesenchymal stem cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene that results in permanent deletion, insertion, correction or modulation of expression or function of one or more mutations within or near or affecting the expression or function of the RAG1 gene or within or near a safe harbor locus that results and restoration of RAG1 protein activity. The safe harbor locus can be selected from the group consisting of: AAVS1 (PPP1R12C), ALB, Angptl3, ApoC3, ASGR2, CCR5, FIX (F9), G6PC, Gys2, HGD, Lp(a), Pcsk9, Serpinal, TF, and TTR. The safe harbor locus can be selected from the group consisting of: exon 1-2 of AAVS1 (PPP1R12C), exon 1-2 of ALB, exon 1-2 of Angptl3, exon 1-2 of ApoC3, exon 1-2 of ASGR2, exon 1-2 of CCR5, exon 1-2 of FIX (F9), exon 1-2 of G6PC, exon 1-2 of Gys2, exon 1-2 of HGD, exon 1-2 of Lp(a), exon 1-2 of Pcsk9, exon 1-2 of Serpinal, exon 1-2 of TF, and exon 1-2 of TTR. In some embodiments, the step of differentiating the genome-edited mesenchymal stem cell into a hematopoietic progenitor cell or white blood cell comprises one or more of the following: treatment with a combination of small molecules or delivery of master transcription factors. In some embodiments, the step of implanting the hematopoietic progenitor cell or white blood cell into the patient comprises implanting the cell into the patient by transplantation, local injection, or systemic infusion, or combinations thereof. In another aspect, provided herein is an ex vivo method for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome comprising the steps of: i) isolating a hematopoietic progenitor cell from the patient; ii) editing the Recombination Activating Gene 1 (RAG1) gene of the hematopoietic progenitor cell, or other DNA sequences that encode regulatory elements of the RAG1 gene, or editing within or near a safe harbor locus of the cell; and iii) implanting the cell into the patient. In some embodiments, the method further comprises treating the patient with granulocyte colony stimulating factor (GCSF) prior to the step of isolating a hematopoietic progenitor cell from the patient. In some embodiments, step of treating the patient with granulocyte colony stimulating factor (GCSF) is performed in combination with Plerixaflor. In some embodiments, the step of isolating a hematopoietic progenitor cell from the patient comprises isolating CD34+ cells. In some embodiments, the step of editing the Recombination Activating Gene 1 (RAG1) gene of the hematopoietic progenitor cell comprises introducing into the progenitor cell one or more deoxyribonucleic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene that results in permanent deletion, insertion, correction, modulation of one or more mutations or exons within or near the RAG1 gene that results in permanent insertion of the RAG1 gene or minigene, and restoration of RAG1 protein activity. In some embodiments, the step of implanting the cell into the patient comprises implanting the progenitor cell into the patient by transplantation, local injection, or systemic infusion, or combinations thereof. In yet another aspect, provided herein is an in vivo method for treating a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome comprising the step of editing the Recombination Activating Gene 1 (RAG1) gene in a cell of the patient. In some embodiments, the step of editing the Recombination Activating Gene 1 (RAG1) gene in a cell of the patient comprises introducing into the cell one or more deoxyribonudeic acid (DNA) endonucleases to effect one or more single-strand breaks (SSBs) or double-strand breaks (DSBs) within or near the RAG1 gene or DNA sequences that encode regulatory elements of the RAG1 gene or editing within or near a safe harbor locus of the RAG1 gene that results in permanent deletion, insertion, correction, or modulation of expression or function of one or more mutations or exons within or near the RAG1 gene and restoration of RAG1 protein activity. In some embodiments, the cell is a bone marrow cell, a hematopoietic progenitor cell, or a CD34+ cell. In some embodiments, the one or more DNA endonucleases is a Cas1, Cas1B, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8, Cas9 (also known as Csn1 and Csx12), Cas100, Csy1, Csy2, Csy3, Cse1, Cse2, Csc1, Csc2, Csa5, Csn2, Csm2, Csm3, Csm4, Csm5, Csm6, Cmr1, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csx17, Csx14, Csx10, Csx16, CsaX, Csx3, Csx1, Csx15, Csf1, Csf2, Csf3, Csf4, or Cpf1 endonuclease; a homolog thereof, recombination of the naturally occurring molecule, codon-optimized, or modified version thereof, and combinations of any of the foregoing. In some embodiments, the method comprises introducing into the cell one or more polynucleotides encoding the one or more DNA endonucleases. In some embodiments, the method comprises introducing into the cell one or more ribonucleic acids (RNAs) encoding the one or more DNA endonucleases. In some embodiments, the one or more polynucleotides or one or more RNAs is one or more modified polynucleotides or one or more modified RNAs. In some embodiments, the method comprises introducing into the cell one or more DNA endonucleases wherein the endonuclease is a protein or polypeptide. In some embodiments, the method further comprises introducing into the cell one or more guide ribonucleic acids (gRNAs). In some embodiments, the one or more gRNAs are single-molecule guide RNA (sgRNAs). In some embodiments, the one or more gRNAs or one or more sgRNAs is one or more modified gRNAs or one or more modified sgRNAs, or combinations thereof. In some embodiments, the one or more DNA endonucleases is pre-complexed with one or more gRNAs or one or more sgRNAs, or combinations thereof. In some embodiments, the method further comprises introducing into the cell a polynucleotide donor template comprising at least a portion of the wild-type RAG1 gene or minigene (comprised of, natural or synthetic enhancer and promoter, one or more exons, and natural or synthetic introns, and natural or synthetic 3′UTR and polyadenylation signal), DNA sequences that encode wild-type regulatory elements of the RAG1 gene, and/or cDNA. In some embodiments, the part of the wild-type RAG1 gene or cDNA is exon 1, exon 2, intronic regions, fragments or combinations thereof, or the entire RAG1 gene or cDNA. In some embodiments, the donor template is either a single or double stranded polynucleotide. In some embodiments, the donor template has homologous arms to the 11p13 region. In some embodiments, the method further comprises introducing into the cell one guide ribonucleic acid (gRNA) and a polynucleotide donor template comprising at least a portion of the wild-type RAG1 gene. In some embodiments, the method further comprises introducing into the cell one guide ribonucleic acid (gRNA) and a polynucleotide donor template comprising at least a portion of a codon optimized or modified RAG1 gene. The one or more DNA endonucleases is one or more Cas9 or Cpf1 endonucleases that effect one single-strand break (SSB) or double-strand break (DSB) at a locus within or near the RAG1 gene (or codon optimized or modified RAG1 gene) or other DNA sequences that encode regulatory elements of the RAG1 gene, or within or near a safe harbor locus that facilitates insertion of a new sequence from the polynucleotide donor template into the chromosomal DNA at the locus or safe harbor locus that results in a permanent insertion or correction of a part of the chromosomal DNA of the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene proximal to the locus or safe harbor locus, and wherein the gRNA comprises a spacer sequence that is complementary to a segment of the locus or safe harbor locus. In some embodiments, proximal means nucleotides both upstream and downstream of the locus or safe harbor locus. In some embodiments, the method further comprises introducing into the cell two guide ribonucleic acid (gRNAs) and a polynucleotide donor template comprising at least a portion of the wild-type RAG1 gene, and wherein the one or more DNA endonucleases is two or more Cas9 or Cpf1 endonucleases that effect a pair of single-strand breaks (SSBs) or double-strand breaks (DSBs), the first at a 5′ locus and the second at a 3′ locus, within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene, or within or near a safe harbor locus that facilitates insertion of a new sequence from the polynucleotide donor template into the chromosomal DNA between the 5′ locus and the 3′ locus that results in permanent insertion or correction of the chromosomal DNA between the 5′ locus and the 3′ locus within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene, or within or near a safe harbor locus and restoration of RAG1 protein activity, and wherein the first guide RNA comprises a spacer sequence that is complementary to a segment of the 5′ locus and the second guide RNA comprises a spacer sequence that is complementary to a segment of the 3′ locus. In some embodiments, the one or more gRNAs are one or more single-molecule guide RNA (sgRNAs). In some embodiments, the one or more gRNAs or one or more sgRNAs is one or more modified gRNAs or one or more modified sgRNAs. In some embodiments, the one or more DNA endonucleases is pre-complexed with one more two gRNAs or one or more sgRNAs. In some embodiments, the part of the wild-type RAG1 gene or cDNA is exon 1, intron 1, exon 2, combinations thereof, or the entire RAG1 gene or cDNA. In some embodiments, the donor template is either a single or double stranded polynucleotide. In some embodiments, the donor template has homologous arms to the 11p13 region. In some embodiments, the locus, or 5′ locus and 3′ locus are in the first or second exon, first intron, or both the first exon and first intron of the RAG1 of the RAG1 gene. In some embodiments, the insertion or correction is by homology directed repair (HDR). In some embodiments, the method further comprises introducing into the cell two guide ribonucleic acid (gRNAs), and wherein the one or more DNA endonucleases is two or more Cas9 or Cpf1 endonucleases that effect a pair of double-strand breaks (DSBs), the first at a 5′ DSB locus and the second at a 3′ DSB locus, within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene, or within or near a safe harbor locus that that causes a deletion of the chromosomal DNA between the 5′ DSB locus and the 3′ DSB locus that results in permanent deletion of the chromosomal DNA between the 5′ DSB locus and the 3′ DSB locus within or near the RAG1 gene or other DNA sequences that encode regulatory elements of the RAG1 gene, or within or near a safe harbor locus and restoration of RAG1 protein activity, and wherein the first guide RNA comprises a spacer sequence that is complementary to a segment of the 5′ DSB locus and the second guide RNA comprises a spacer sequence that is complementary to a segment of the 3′ DSB locus. In some embodiments, the two gRNAs are two single-molecule guide RNA (sgRNAs). In some embodiments, the two gRNAs or two sgRNAs are two modified gRNAs or two modified sgRNAs. In some embodiments, the one or more DNA endonucleases is pre-complexed with one or two gRNAs or one or two sgRNAs. In some embodiments, both the 5′ DSB and 3′ DSB are in or near either the first exon, first intron, or second exon of the RAG1 gene. In some embodiments, the correction is by homology directed repair (HDR). In some embodiments, the correction is by non-homologous end joining (NHEJ). In some embodiments, the deletion is a deletion of 1 kb or less. In some embodiments, the Cas9 or Cpf1 mRNA, gRNA, and donor template are either each formulated separately into lipid nanoparticles or all co-formulated into a lipid nanoparticle. In some embodiments, the Cas9 or Cpf1 mRNA, gRNA, and donor template are formulated into separate exosomes or are co-formulated into an exosome. In some embodiments, the Cas9 or Cpf1 mRNA is formulated into a lipid nanoparticle, and both the gRNA and donor template are delivered to the cell by a viral vector. In some embodiments, the viral vector is an adeno-associated virus (AAV) vector. In some embodiments, the AAV vector is an AAV6 vector. The Cas9 or Cpf1 mRNA can be formulated into a lipid nanoparticle, and the gRNA can be delivered to the cell by electroporation and donor template can be delivered to the cell by a viral vector. In some embodiments, the viral vector is an adeno-associated virus (AAV) vector. In some embodiments, the AAV vector is an AAV6 vector. In some embodiments, the gRNA is delivered to the cell by electroporation and donor template is delivered to the cell by an adeno-associated virus (AAV) vector. In some embodiments, the AAV vector is an AAV6 vector. In some embodiments, the RAG1 gene is located on Chromosome 11: 36,510,372-36,593,156 (Genome Reference Consortium—GRCh38/hg38). In some embodiments, the RAG1 gene is located within a location on Chromosome 11, plus or minus 3 KB on either end: 36568013-36579760 (Genome Reference Consortium—GRCh38/hg38). In some embodiments, the RAG1 gene is located on Chromosome 11: 36568013-36579760 (Genome Reference Consortium—GRCh38/hg38). The restoration of RAG1 protein activity can be compared to wild-type or normal RAG1 protein activity. In another aspect, provided herein is one or more guide ribonucleic acids (gRNAs) comprising a spacer sequence selected from the group consisting of the nucleic acid sequences in SEQ ID NOs: 54,860-66,285 editing the RAG1 gene in a cell from a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome. In some embodiments, the one or more gRNAs are one or more single-molecule guide RNAs (sgRNAs). In some embodiments, the one or more gRNAs or one or more sgRNAs is one or more modified gRNAs or one or more modified sgRNAs. In another aspect, provided herein is one or more guide ribonucleic acids (gRNAs) comprising a spacer sequence selected from the group consisting of the nucleic acid sequences in SEQ ID NOs: 1-54,859 for editing a safe harbor locus in a cell from a patient with severe combined immunodeficiency (SCID) or Omenn Syndrome, wherein the safe harbor locus is selected from the group consisting of AAVS1 (PPP1R12C), ALB, Angptl3, ApoC3, ASGR2, CCR5, FIX (F9), G6PC, Gys2, HGD, Lp(a), Pcsk9, Serpinal, TF, and TTR. In some embodiments, the one or more gRNAs are one or more single-molecule guide RNAs (sgRNAs). In some embodiments, the one or more gRNAs or one or more sgRNAs is one or more modified gRNAs or one or more modified sgRNAs. In another aspect, provided herein are cells that have been modified by the preceding methods to permanently correct one or more mutations within the RAG1 gene and restore RAG1 protein activity. Further provided herein are methods for ameliorating severe combined immunodeficiency (SCID) or Omenn Syndrome by the administration of cells that have been modified by the preceding methods to a SCID or Omenn Syndrome patient. In some embodiments, the methods and compositions of the disclosure comprise one or more modified guide ribonucleic acids (gRNAs). Non-limiting examples of modifications can comprise one or more nucleotides modified at the 2′ position of the sugar, in some embodiments a 2′-O-alkyl, 2′-O-alkyl-O-alkyl, or 2′-fluoro-modified nucleotide. In some embodiments, RNA modifications include 2′-fluoro, 2′-amino or 2′ O-methyl modifications on the ribose of pyrimidines, abasic residues, desoxy nucleotides, or an inverted base at the 3′ end of the RNA. In some embodiments, the one or more modified guide ribonucleic acids (gRNAs) comprise a modification that makes the modified gRNA more resistant to nuclease digestion than the native oligonucleotide. Non-limiting examples of such modifications include those comprising modified backbones, for example, phosphorothioates, phosphorothyos, phosphotriesters, methyl phosphonates, short chain alkyl or cycloalkyl intersugar linkages or short chain heteroatomic or heterocyclic intersugar linkages. Various other aspects are described and exemplified herein. BRIEF DESCRIPTION OF THE DRAWINGS Various aspects of materials and methods for treatment of severe combined immunodeficiency (SCID) or Omenn Syndrome disclosed and described in this specification can be better understood by reference to the accompanying figures, in which: FIG. 1A is an illustration depicting the type II CRISPR/Cas system. FIG. 1B is another illustration depicting the type II CRISPR/Cas system. FIG. 2 is a graph depicting cutting efficiencies of gRNAs transcribed in vitro and transfected in primary human mobilized Peripheral Blood CD34+ cells (mPB CD34) that constitutively express Cas9, as evaluated using TIDE analysis. BRIEF DESCRIPTION OF THE SEQUENCE LISTING SEQ ID NOs: 1-2,032 are 20 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 2,033-2,203 are 20 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 2,204-2,221 are 20 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 2,222-2,230 are 20 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 2,231-2,305 are 20 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 2,306-3,481 are 22 bp spacer sequences for targeting exons 1-2 of an AAVS1 (PPP1R12C) gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 3,482-3,649 are 20 bp spacer sequences for targeting exons 1-2 of an Alb gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 3,650-3,677 are 20 bp spacer sequences for targeting exons 1-2 of an Alb gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 3,678-3,695 are 20 bp spacer sequences for targeting exons 1-2 of an Alb gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 3,696-3,700 are 20 bp spacer sequences for targeting exons 1-2 of an Alb gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 3,701-3,724 are 20 bp spacer sequences for targeting exons 1-2 of an Alb gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 3,725-4,103 are 22 bp spacer sequences for targeting exons 1-2 of an Alb gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 4,104-4,448 are 20 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 4,449-4,484 are 20 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 4,485-4,507 are 20 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 4,508-4,520 are 20 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 4,521-4,583 are 20 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 4,584-5,431 are 22 bp spacer sequences for targeting exons 1-2 of an Angpt13 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 5,432-5,834 are 20 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 5,835-5,859 are 20 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 5,860-5,862 are 20 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 5,863-5,864 are 20 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 5,865-5,876 are 20 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 5,877-6,108 are 22 bp spacer sequences for targeting exons 1-2 of an ApoC3 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 6,109-7,876 are 20 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 7,877-8,082 are 20 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 8,083-8,106 are 20 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 8,107-8,118 are 20 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 8,119-8,201 are 20 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 8,202-9,641 are 22 bp spacer sequences for targeting exons 1-2 of an ASGR2 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 9,642-9,844 are 20 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 9,845-9,876 are 20 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 9,877-9,890 are 20 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 9,891-9,892 are 20 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 9,893-9,920 are 20 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 9,921-10,220 are 22 bp spacer sequences for targeting exons 1-2 of a CCR5 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 10,221-11,686 are 20 bp spacer sequences for targeting exons 1-2 of an F9 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 11,687-11,849 are 20 bp spacer sequences for targeting exons 1-2 of an F9 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 11,850-11,910 are 20 bp spacer sequences for targeting exons 1-2 of an F9 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 11,911-11,935 are 20 bp spacer sequences for targeting exons 1-2 of an F9 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 11,936-12,088 are 20 bp spacer sequences for targeting exons 1-2 of an F9 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 12,089-14,229 are 22 bp spacer sequences for targeting exons 1-2 of an F9 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 14,230-15,245 are 20 bp spacer sequences for targeting exons 1-2 of a G6PC gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 15,246-15,362 are 20 bp spacer sequences for targeting exons 1-2 of a G6PC gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 15,363-15,386 are 20 bp spacer sequences for targeting exons 1-2 of a G6PC gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 15,387-15,395 are 20 bp spacer sequences for targeting exons 1-2 of a G6PC gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 15,396-15,485 are 20 bp spacer sequences for targeting exons 1-2 of a G6PC gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 15,486-16,580 are 22 bp spacer sequences for targeting exons 1-2 of a G6PC gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 16,581-22,073 are 20 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 22,074-22,749 are 20 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 22,750-23,027 are 20 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 23,028-23,141 are 20 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 23,142-23,821 are 20 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 23,822-32,253 are 22 bp spacer sequences for targeting exons 1-2 of a Gys2 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 32,254-33,946 are 20 bp spacer sequences for targeting exons 1-2 of an HGD gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 33,947-34,160 are 20 bp spacer sequences for targeting exons 1-2 of an HGD gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 34,161-34,243 are 20 bp spacer sequences for targeting exons 1-2 of an HGD gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 34,244-34,262 are 20 bp spacer sequences for targeting exons 1-2 of an HGD gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 34,263-34,463 are 20 bp spacer sequences for targeting exons 1-2 of an HGD gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 34,464-36,788 are 22 bp spacer sequences for targeting exons 1-2 of an HGD gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 36,789-40,583 are 20 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 40,584-40,993 are 20 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 40,994-41,129 are 20 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 41,130-41,164 are 20 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 41,165-41,532 are 20 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 41,533-46,153 are 22 bp spacer sequences for targeting exons 1-2 of an Lp(a) gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 46,154-48,173 are 20 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 48,174-48,360 are 20 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 48,361-48,396 are 20 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 48,397-48,410 are 20 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 48,411-48,550 are 20 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 48,551-50,344 are 22 bp spacer sequences for targeting exons 1-2 of a PCSK9 gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 50,345-51,482 are 20 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 51,483-51,575 are 20 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 51,576-51,587 are 20 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 51,588-51,590 are 20 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 51,591-51,641 are 20 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 51,642-52,445 are 22 bp spacer sequences for targeting exons 1-2 of a Serpinal gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 52,446-53,277 are 20 bp spacer sequences for targeting exons 1-2 of a TF gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 53,278-53,363 are 20 bp spacer sequences for targeting exons 1-2 of a TF gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 53,364-53,375 are 20 bp spacer sequences for targeting exons 1-2 of a TF gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 53,376-53,382 are 20 bp spacer sequences for targeting exons 1-2 of a TF gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 53,383-53,426 are 20 bp spacer sequences for targeting exons 1-2 of a TF gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 53,427-54,062 are 22 bp spacer sequences for targeting exons 1-2 of a TF gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 54,063-54,362 are 20 bp spacer sequences for targeting exons 1-2 of a TTR gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 54,363-54,403 are 20 bp spacer sequences for targeting exons 1-2 of a TTR gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 54,404-54,420 are 20 bp spacer sequences for targeting exons 1-2 of a TTR gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 54,421-54,422 are 20 bp spacer sequences for targeting exons 1-2 of a TTR gene with a T. denticola Cas9 endonuclease. SEQ ID NOs: 54,423-54,457 are 20 bp spacer sequences for targeting exons 1-2 of a TTR gene with a N. meningitides Cas9 endonuclease. SEQ ID NOs: 54,458-54,859 are 22 bp spacer sequences for targeting exons 1-2 of a TTR gene with an Acidominococcus, Lachnospiraceae, and Francisella novicida Cpf1 endonuclease. SEQ ID NOs: 54,860-59,105 are 20 bp spacer sequences for targeting exons 1-2 of a Recombination Activating Gene 1 (RAG1) gene with a S. pyogenes Cas9 endonuclease. SEQ ID NOs: 59,106-59,602 are 20 bp spacer sequences for targeting exons 1-2 of a Recombination Activating Gene 1 (RAG1) gene with a S. aureus Cas9 endonuclease. SEQ ID NOs: 59,603-59,759 are 20 bp spacer sequences for targeting exons 1-2 of a Recombination Activating Gene 1 (RAG1) gene with a S. thermophilus Cas9 endonuclease. SEQ ID NOs: 59,760-59,824 are 20 bp spacer sequences for targeting exons 1-2 of
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