Cardiotropic cMet+ T cells are significantly increased in the blood and the myocardium of patients with acute myocarditis as well as in mice with experimental autoimmune myocarditis.35 The phenotype and function of cMet+ T cells were distinct from those of cMet− T cells, including preferential proliferation to cardiac autoantigens (cardiac myosin heavy chain [MHCα6 peptide]) and coproduction of multiple cytokines (IL-4, IL-17, and IL-22). This evidence concerns the gene IL22 and myocarditis.