CD8A and myocarditis: This immunological tolerance appears to be critically disrupted by ICIs, particularly PD-1/PD-L1 blockade: in their pivotal work, Moslehi et al. demonstrated that genetic deletion or pharmacologic inhibition of PD-1 leads to spontaneous myocarditis in murine models, characterized by diffuse CD8+ T-cell infiltration and myocardial necrosis [9,33,34,35].