In murine models of doxorubicin (DOX) and ischemia/reperfusion (I/R)-induced cardiomyopathy, administering DOX to mice induced cardiomyopathy with a rapid, systemic accumulation of non-heme iron via heme degradation by Nrf2-mediated upregulation of HO-1, which effect was abolished in Nrf2-deficient mice (Fang et al., 2019). The gene discussed is HMOX1; the disease is cardiomyopathy.