In MRL-lpr−/− mice (lacking FAS and predisposed to the development of systemic lupus erythematosus (SLE)-like phenotype), deletion of PD-1/PD-1L or the administration of neutralizing antibodies resulted in autoimmune myocarditis and CD4/8 infiltration; however, unlike in human ICI myocarditis, substantial levels of autoantibody formation against myosin were detected [173,183]. This evidence concerns the gene CD4 and myocarditis.