Ideally, further optimization efforts will improve the potency of MN1.4 while maintaining agonism, and the resulting optimized peptides will undergo testing in mouse models of diseases caused by deficient PD-1 signaling, such as C57BL/6 PD-1−/− mice that have been used to study PD-1 deficiency in the context of lupus-like disease and type 1 diabetes (3, 30). The gene discussed is PDCD1; the disease is type 1 diabetes mellitus.