This conclusion is firstly supported by the observations that treatment with HO-1 inducer Hemin or infection of HO-1 adenovirus prevented H2O2-induced expression of cell senescence marker SA-β-gal, upregulation of cell cycle inhibitor p53 and p21, as well as increase of phosphorylated γH2A.X level which indicates DNA damage and telomere dysfunction. The gene discussed is TP53; the disease is infection.