It is well established that autoimmune disorders are characterized by elevated T helper 1 (Th1) and T helper 17 (Th17) cell activity, accompanied by increased Interferon-gamma (IFN-γ) release due to the epigenetic modifications; gain or loss of the histone modification and DNA methylation lead to the production of Th0, Th1, and Th2 lineages [56]. The gene discussed is IFNG; the disease is autoimmune disease.