Here is emerging evidence to indicate that m6A modification is closely related to the occurrence and progression of CVDs, including cardiac hypertrophy, heart failure, ischemic heart disease, etc. Dorn et al. [10] demonstrated that METTL3-mediated m6A modification is significant for maintaining cardiac homeostasis and normal cardiac function and revealed increased m6A methylation in cardiomyocytes under hypertrophic stimulation. Here, METTL3 is linked to coronary artery disorder.