METTL3 and myocardial infarction: We demonstrated that METTL3/m6A was upregulated in microglia of PVN in MI rats, m6A installation on TLR4 mRNA 3'UTR region was increased mediated by METTL3 and enhanced TLR4 expression in the PVN combined with activated NF‐κB signalling led to the overwhelming production of pro‐inflammatory cytokines during MI, consequently, sympathetic activation initiated arrhythmia after MI (Figure 7).