The tumor progression in hairless mice was very similar to that in humans starting with endophytically growing actinic keratosis as benign precursor lesions (majority of tumors <2 mm across) of which a fraction progressed to malignant SCCs (majority > 3 mm) (44), and with a majority throughout bearing UV signature mutations in the tumorsuppressor p53 (46); even before tumors appeared, microscopic clusters overexpressing mutant-p53 could be detected in the chronically sub-sunburn UV-exposed skin (47). Here, TP53 is linked to actinic keratosis.