Consistently, impaired PINK1 and Parkin-mediated mitophagy affected by Parkin deficiency or mutations in MFN2 results in the retention of fetal cardiac mitochondria, reduced oxidative metabolism, heart failure, and premature death (Chen and Dorn, 2013; Gong et al., 2015), highlighting that mitophagy underlies mitochondrial plasticity and metabolic transitioning in developing cardiomyocytes. The gene discussed is PRKN; the disease is heart failure.