However, the study of DMBA/PMA-induced carcinogenesis in a mouse skin model (with or without a p53+/− background) that artificially overexpresses survivin in skin using a skin-specific keratin-14 gene promoter, paradoxically revealed that tumour formation was less frequent and significantly delayed in survivin-Tg mice in comparison with non-Tg littermates, although Tg mice promote papilloma progression into SCC after tumours are initiated from DMBA/PMA treatment. This evidence concerns the gene TP53 and papilloma.