PD-1:PD-L1 signals are thought to be indispensable for the prevention of T1D, whereas PD-1:PD-L2 signals are not, because (1) PD-1- and PD-L1-deficient NOD mice develop rapid-onset autoimmune diabetes, whereas PD-L2-deficient NOD mice do not (Keir et al., 2006; Wang et al., 2005); and (2) the antibody-mediated blockade of PD-1 or PD-L1, but not that of PD-L2 or CTLA-4, induces autoimmune diabetes in NOD mice (Ansari et al., 2003). The gene discussed is CTLA4; the disease is type 1 diabetes mellitus.