Mettl3 enhances oxLDL‐triggered inflammation through promoting STAT1 expression in m6A‐dependent manner, and Mettl3 interacts with STAT1 to promote STAT1 transcriptional regulation of inflammatory factor expression in RAW264.7 macrophages, which was also demonstrated in the monocytes from patients with angiographically proven CAD, suggesting that Mettl3 may be a potential target for the clinical treatment of AS. This evidence concerns the gene METTL3 and coronary artery disorder.