In myocardial infarction models, METTL3-mediated m6A modification within microglia activates the TRAF6/ECSIT signaling pathway, induces mitochondrial oxidative stress in PVN neurons, and stimulates sympathetic hyperactivity, thereby contributing to the development of post-MI ventricular arrhythmias [130,141]. This evidence concerns the gene TRAF6 and myocardial infarction.