Using a skin carcinogenesis model, it was found that 7,12-dimethylbenz[a]anthracene (DMBA) and tetradecanoylphorbol-13-acetate (TPA) activate p53 during tumor initiation and lead to SOD2 transcriptional repression, via inhibition of Sp1 binding to the proximal promoter [22,91]. The gene discussed is SOD2; the disease is neoplasm.