There is ample evidence yielded from non-obese diabetic (NOD) mice indicating that the disinhibition of the interaction between PD-1 expressed on activated T cells and PD-L1 expressed on β cells—but not the disinhibition of the CTLA-4 or of the PD-L2—unleashes the proliferation and the pancreatic infiltration of self-reactive T cells concerning both CD4+ T and CD8+ T cells, thereby causing autoimmune β-cell destruction that results in T1DM [10,11]. This evidence concerns the gene PDCD1 and type 1 diabetes mellitus.