thought to be an epigenetic cause of T2DM by causing the body to develop an insulin resistance and inhibit the production of beta cells in the pancreas. Because of the repressed genes the body does not regulate blood sugar transport to cells, causing a high concentration of glucose in the blood stream. Another variation of T2DM is mitochondrial reactive oxygen species (ROS) which causes a lack of antioxidants in the blood. This leads to oxidation stress of cells leading to the release of free radicals inhibiting blood glucose regulation and hyperglycemic conditions. This leads to persistent vascular complications that can inhibit blood flow to limbs and the eyes. This persistent hyperglycemic environment is leads to DNA methylation as well because the chemistry within chromatin in the nucleus is affected. Current medicine used by T2DM sufferers includes Metformin hydrochloride which stimulates production in the pancreas and promotes insulin sensitivity. A number of preclinical studies have suggested that adding a treatment to metformin that would inhibit acetylation and methylation of DNA and histone complexes. DNA methylation occurs throughout the human genome and is believed to be a natural method of suppressing genes during development. Treatments targeting specific genes with methylation and acetylation inhibitors is being studied and debated. With Exposure therapy for Fear, anxiety, and trauma Traumatic experiences can lead to a number of mental problems including posttraumatic stress disorder. It was previously thought that PTSD could be treated with advances in cognitive behavioral therapy methods like Exposure therapy. In exposure therapy, patients are exposed to stimuli which provokes fear and anxiety. In theory, repeated exposure can led to a decreased connection between the stimuli and the anxiety. While exposure therapy helps many patients, there are many patients who do not experience improvement in their symptoms while others may experience more symptoms. The biochemical mechanisms underlying these systems are not completely understood. However, brain-derived neurotrophic factor (BDNF) and the N-methyl-D-aspartate receptors (NMDA) have been identified as crucial in the exposure therapy process. Successful exposure therapy is associated with increased acetylation of these two genes, leading to transcriptional activation of these genes, which appears to increase neural plasticity. For these reasons, increasing the acetylation of these two genes has been a major area of recent research into the treatment of anxiety disorders. Exposure therapy’s effectiveness in rodents is increased by the administration of Vorinostat, Entinostat, TSA, sodium butyrate, and VPA, all known histone