These included hypomethylation of HLA class II gene, HLA-DQB1, which carries the highest single genetic risk for T1DM (along with HLA-DRB1), hypomethylation of RFXAP, an HLA class II regulating element, hypomethylation of NFKB1A, an important regulator of apoptosis and inflammatory immune responses, and hypomethylation of GAD2 which encodes GAD65, a major T1DM autoantigen involved in disease etiology. This evidence concerns the gene GAD2 and type 1 diabetes mellitus.