The recombinant MG-53 improved cardiac functions in mouse and pig models of MI by reducing mitochondrial reactive oxygen species production, preserving mitochondrial membrane potential, and decreasing mitophagy in cardiomyocytes [23]. Most of the MG-53’s functions were from animal studies, and there were limited human studies to support the findings, so the transition of MG-53’s functions to humans should be taken cautiously. Here, TRIM72 is linked to myocardial infarction.