Recent studies show that IFN‐γ‐producing CD8+ T cells induce the expansion of a monocyte‐derived Cxcl9+Cxcl10+ macrophage subset to potentiate myocardial inflammation and remodeling; while, blocking IFN‐γ signaling can alleviate ICI myocarditis.[201, 202] In autoimmune myocarditis, Th17 cell‐derived IL‐17A is dispensable for the development of myocarditis. This evidence concerns the gene IFNG and autoimmune myocarditis.