In particular, we demonstrate the following: evidence of defective 8oxoG BER in human plaque VSMCs, not just increased damage or reduced expression of BER enzymes; that reducing physiological 8oxoG levels reduces atherosclerosis, in addition to the detrimental effects of artificially elevated 8oxoG; the importance of OGG1 acetylation to its function in vivo; that SIRT1 regulates OGG1 acetylation in vivo; and that p300 regulates OGG1 stability, not just activity. This evidence concerns the gene SIRT1 and atherosclerosis.