IL‐4 and IL‐13 have been shown to exert powerful profibrotic effects within the heart, liver, intestines, and lungs7, 8, 9 and have been implicated in various chronic fibrotic diseases.31 In contrast, Il13‐deficient male mice display increased cardiac fibrosis in models of myocarditis and myocardial infarction.10, 11 Based on our findings, it may now be possible to resolve these seemingly contradictory findings. The gene discussed is IL4; the disease is myocarditis.