In our mouse model, anti-PD-1 mAb treatment seems to directly activate autoreactive T cells targeting the heart by blocking the inhibitory PD-1/PD-L1 pathway, leading to the excessive production of effector cytokines and cytotoxic molecules such as IFN-γ, perforin, and granzyme B followed by myocardial damage and myocarditis development (138). The gene discussed is PDCD1; the disease is myocarditis.