Similar to plaque VSMCs,22,23 senescent cells acquire a glycolytic24,25 and highly inflammatory state and may promote atherosclerosis via their senescence-associated secretory phenotype.26 In some cell types, SIRT6 can epigenetically control glucose11 and fatty acid12,13 metabolism, and NF-κB-dependent inflammation.9 In contrast, we find that SIRT6 does not transcriptionally regulate glycolysis, FAO and proinflammatory cytokine expression in proliferating hVSMCs, and NF-κB is not activated in senescent SIRT6-depleted hVSMCs. This evidence concerns the gene NFKB1 and atherosclerosis.