Despite the continued gaps in our understanding of the precise mechanisms(s) by which aberrant fission-fusion contributes to IR-induced cardiomyocyte death, the data raise the intriguing possibility that the development of pharmacologic agents capable of targeting DRP1-mediated fission, DRP1-associated MOMP, and/or loss of cristae integrity may potentially provide novel strategies to attenuate lethal ischemia-reperfusion injury and improve outcomes in patients post-MI. Here, DNM1L is linked to myocardial infarction.