DOX-treated mice up-regulate the expression of heme oxygenase-1 (Hmox-1), leading to heme degradation in heart and release of free iron, which accumulates in mitochondria rapidly and causes myocardial damage (Fang et al., 2019), while Fer-1 and Lip-1 can reduce the cardiotoxicity induced by doxorubicin (DOX) (Fang et al., 2019; Koleini et al., 2019), suggesting that ferroptosis plays an important role in DOX-induced HF. Here, HMOX1 is linked to hydrops fetalis.