Research has demonstrated that SIRT1 deficiency caused over-acetylation of eNOS, resulting in functional inactivation of eNOS, which further promoted the development of atherosclerotic plaques in mice, while HDAC3-mediated Lys610 deacetylation of eNOS promoted the atherosclerosis process (Jung et al., 2010; Yang et al., 2017; Rössig et al., 2002; Schermuly et al., 2011). The gene discussed is SIRT1; the disease is atherosclerosis.