The ablation of Mfn2 in mouse cardiomyocytes prevents the depolarization-induced translocation of parkin to the mitochondria and suppresses mitophagy (Chen and Dorn, 2013), and the downregulation of Mfn2 causes an imbalance in mitochondrial dynamics, which leads to mitochondrial dysfunction and ultimately contributes to the development of DCM (Hu et al., 2019). This evidence concerns the gene PRKN and familial dilated cardiomyopathy.