Furthermore, the findings from independent studies, which highlight the involvement of cardiac myosin heavy chain-reactive T cells in the development of ICI myocarditis, emphasize the critical function of immune checkpoint molecules, such as PD-1/PD-L1 and CTLA-4, in maintaining cardiac autoimmunity under normal conditions (Figure 1) (147). The gene discussed is CTLA4; the disease is myocarditis.