Severe myocarditis occurring in the absence of IL-13, characterized by increased leukocyte infiltration of myocardial tissues, increased levels of pro-inflammatory IL-1b and IL-18 (but not IL-17), increased levels of autoantibodies to cardiac myosin and severe cardiac fibrosis was considered as the development of severe dilated cardiomyopathy with impaired cardiac function in IL-13 knockout mice and was fatal in most cases. The gene discussed is IL17A; the disease is dilated cardiomyopathy.