Our previous study showed that lentiviral expression of Δ133p53α delayed the onset of cellular senescence and reduced the production of the proinflammatory cytokine IL-6 in fibroblasts derived from HGPS patients, concurrent with mitigated DNA damage and repressed expression of p21WAF1, a p53-inducible gene that mediates cellular senescence [7]. Here, TP53 is linked to Hutchinson-Gilford progeria syndrome.