Cardiomyocyte death is a pathological feature of DOX‐induced myocardial damage and cardiac dysfunction.[19] The emerging form of cell death, ferroptosis, is one of the principal pathogenic mechanisms of cancer,[20] ischemic organ damage,[21] and other degenerative diseases closely related to lipid peroxidation.[22] Substantial evidence indicates that inhibition of cardiomyocyte ferroptosis is a promising preventative therapeutic strategy for DIC.[7, 23] However, it remains unclear whether PrA regulates DOX‐mediated ferroptosis in cardiomyocytes. The gene discussed is S100A6; the disease is cancer.