For instance, cytotoxic CD8 + T cells, particularly the TEMRA subset (TEMRA cells are terminally differentiated effector T cells that are associated with protracted antigen exposure) have been implicated in ICI-induced myocarditis due to their clonal expansion and cytotoxic activity within the myocardium [49].Macrophages also play a significant role, with an expansion of inflammatory CCR2 + macrophages observed in myocarditis, driven by interactions with CD8 + T cells and IFN-γ signaling [50]. This evidence concerns the gene CD8A and myocarditis.