The inhibition of SAH hydrolase (SAHH) leads to the accumulation of SAH and the inhibition of DNMT3b (DNA methyltransferase 3b), which results in hypomethylation of the H19 promoter and reduced intracellular adenosine levels, combined with reduced activation of AMPK (AMP-activated protein kinase), which in turn inhibits SIRT1 mediated-hyperacetylation of histone H3 to promote atherosclerosis [130]. This evidence concerns the gene SIRT1 and atherosclerosis.