Senescent VSMCs may promote atherosclerosis at least, in part, via upregulation of inflammatory cytokines, as part of the senescence-associated secretory phenotype.26 SIRT6 exerts anti-inflammatory effects by repressing NF-κB (nuclear factor-κB)-dependent inflammatory gene expression through H3K9 deacetylation at chromatin,9 and loss of SIRT6 triggers NF-κB-dependent senescence in HeLa cells; we, therefore, investigated whether SIRT6 regulates inflammation in hVSMCs. This evidence concerns the gene NFKB1 and atherosclerosis.