mtDNA mutations selectively disrupt the differentiation-induced activation of mitophagy in adult cardiac precursor cells (CPCs), and loss of Bcl-2 interacting protein 3 like (BNIP3L) and FUN14 domain containing 1- (FUNDC-1-) mediated mitophagy during differentiation in CPCs leads to sustained mitochondrial fission and an increased risk of myocardial infarction (MI) [55]. The gene discussed is BNIP3L; the disease is myocardial infarction.