TLR4 and myocardial infarction: The main findings were as follows: (a) Total m6A and METTL3 were highly expressed in rat PVN after MI, and METTL3 was primarily distributed in microglia of PVN in MI rats; (b) TLR4 mRNA expression was upregulated by METTL3‐mediated m6A modification and TLR4/NF‐κB served as the downstream signalling pathway in modulating central sympathetic activation initiated by MI; (c) Targeting METTL3 protected the heart from arrhythmia attack by reducing the sympathetic hyperactivity and reduced infarct size post‐MI.