As previous publications revealed that Sirt1 and Sirt3 were capable of suppressing ROS accumulation through inhibiting the activities of Nox and activating the Mnsod in ageing and carcinogenesis [37–39], we hypothesized that Sirt1 and Sirt3 might also serve as upstream molecules to regulate Nox2 and Mnsod expression in VSMCs during atherosclerosis. Here, SOD2 is linked to atherosclerosis.