Our previous work found that a subpopulation of senescent β cells accumulates during the development of T1D in nonobese diabetic (NOD) mice and humans and expresses DNA damage response (DDR) marker gamma-H2A.X, cyclin-dependent kinase inhibitors Cdkn1a (p21) and Cdkn2a (p16INK4A), SASP markers and a Bcl-2-mediated prosurvival phenotype (14). This evidence concerns the gene BCL2 and type 1 diabetes mellitus.