Knockdown of USP39 can effectively inhibit oxidative stress, inflammation and apoptosis in cardiomyocytes and ameliorate cardiac damage caused by acute myocardial infarction by regulating the USP39/miR-362-3p/TRAF3 axis, resulting in the downregulation of TRAF3 (90). This evidence concerns the gene USP39 and acute myocardial infarction.