In contrast, HDAC1 has been shown to mediate homocysteine-induced atherosclerosis by reducing the acetylation level of histone H3 at lysine 9 (H3K9ac), leading to the accumulation of total cholesterol (TC), free cholesterol, and triglycerides and accelerating the progression of atherosclerosis (Zhao et al., 2017). This evidence concerns the gene HDAC1 and atherosclerosis.