Deficiencies in METTL3 and METTL14 significantly attenuated Ang II–induced myocardial inflammation and fibrosis by reducing m6A modifications on MyD88 and TGF-β1 mRNAs. This reduction inhibited NF-κB pathway activation and decreased the expression of CXCR2 and TGF-β1. This evidence concerns the gene METTL3 and myocarditis.