Meaningfully, and as mentioned above, the expression of α-MyHC is missing in both, humans and mouse mTECs, leading to a defect in negative selection of alpha-myosin heavy chain-specific CD4+ T cells in the thymus putting them at risk for autoimmune myocarditis development in the presence of self-antigen release and innate immune activation (Figure 1). This evidence concerns the gene CD4 and autoimmune myocarditis.