In sepsis‐induced cardiomyopathy, MG53 enhances myocardial performance and attenuates structural injury, partly through exosome‐mediated circRNA regulation, whereas in hypertrophic cardiomyopathy, MG53 stabilizes potassium channel function to counteract arrhythmogenic remodeling [293, 294, 295]. This evidence concerns the gene TRIM72 and hypertrophic cardiomyopathy.