Previous studies have demonstrated that patients with dilated cardiomyopathy (DCM) have higher levels of DRP1 expression and ser 616 phosphorylation, and that DRP1 may also have a role in mediating mitochondrial fission in Dox-induced cardiotoxicity (Catanzaro et al., 2019). This evidence concerns the gene DNM1L and familial dilated cardiomyopathy.