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N 6 -methyladenosine (m 6 A) modification is a newly discovered regulatory mechanism in eukaryotes. As one of the most common epigenetic mechanisms, m 6 A's role in the development of atherosclerosis (AS) and atherosclerotic diseases (AD) has also received increasing attention. Herein, we elucidate the effect of m 6 A on major risk factors for AS, including lipid metabolism disorders, hypertension, and hyperglycemia. We also describe how m 6 A methylation contributes to endothelial cell injury, macrophage response, inflammation, and smooth muscle cell response in AS and AD. Subsequently, we illustrate the m 6 A-mediated aberrant biological role in the pathogenesis of AS and AD, and analyze the levels of m 6 A methylation in peripheral blood or local tissues of AS and AD, which helps to further discuss the diagnostic and therapeutic potential of m 6 A regulation for AS and AD. In summary, studies on m 6 A methylation provide new insights into the pathophysiologic mechanisms of AS and AD, and m 6 A methylation could be a novel diagnostic biomarker and therapeutic target for AS and AD.