However, HDAC3-mediated deacetylation of eNOS K610 promoted atherosclerosis.91–93 The level of inducible nitric oxide synthase (iNOS) is also increased in atherosclerotic lesions.94 In endothelial cells, nuclear factor-κB (NF-κB) promotes atherosclerosis by driving the expression of Nos2(encoding iNOS) and proinflammatory genes.95 SIRT1 inhibits NF-κB activity by deacetylating P65 and eliminating the interaction between P300 and NF-κB.96 It has been reported that lysine acetylation can regulate myocardium ischemia–reperfusion injury and myocardial infarction. This evidence concerns the gene NFKB1 and Atherosclerotic lesion.