Type 1 diabetes is an autoimmune disease that results from autoreactive destruction of insulin producing beta cells and the pathogenesis is characterized by chronic infiltration of immune cells in islets. Stimulator of interferon genes (STING), is a central hub for cytosolic nucleic acid sensing in innate immunity and plays an important role in viral and tumor immunity. Recently, it was reported that gain-of-function mutations in STING cause systemic vasculitis with lupus-like manifestations in human, suggesting that dysregulated type I IFN production via STING contributes to the development of autoimmunity. We recently showed that the presence of aberrant cytosolic DNA can induce production of type I IFN and break immune tolerance in a mouse model of type 1 diabetes. We hypothesis that the STING pathway is involved, by sensing the cytosolic DNA resulting in increased type I IFN. To elucidate whether STING is involved in the pathogenesis of type 1 diabetes, we generated NOD mice deficient in STING by Crispr/Cas9 editing technology. STING-deficient mice have similar proportions of immune cell populations in spleen, thymus and lymph nodes when compared to wild-type NOD mice. Interestingly, STING-deficient NOD mice had increased proportion of CD44+ beta cell antigen-specific T cells, suggesting that contrary to our hypothesis, STING deficiency may increase diabetogenic cells. In support of this, recently STING was shown to have intrinsic anti-proliferative activity in T lymphocytes. Future results will show cumulative diabetes incidence and insulitis, as well as insulin autoantibodies in STING deficient mice.