Previous studies have reported that highly expressed Drp1 and Drp1-dependent excessive mitochondrial fission contributed to DOX-induced cardiomyopathy (Xia et al., 2017; Liang et al., 2020; Zhuang et al., 2021), and Drp1 heterozygous knockout mice were protected against DOX-induced cardiotoxicity (Catanzaro et al., 2019), strongly supporting the critical role of Drp1-dependent mitochondrial fission in DOX-related cardiotoxicity. The gene discussed is DNM1L; the disease is cardiomyopathy.