In particular, the following three mechanisms appear to be of particular importance in the context of the occurrence of ICI-associated cardiovascular toxicities: (1) Impairment of CTLA-4, PD-L1, PD-1, and LAG-3 signaling by ICIs, thereby lowering the threshold for T-cell activation, and (2) the presence of shared antigens between tumor and heart muscle can lead to the infiltration of activated T cells, macrophages, and monocytes into the heart. This evidence concerns the gene PDCD1 and neoplasm.