In mice without p53, cells do not arrest after mutagenesis, and these mice have a high incidence of tumors. DNA damage is monitored by p53, a transcription factor that becomes active in the presence of double-stranded DNA breaks. It activates the transcription of p21 which prohibits the cell cycle by inactivating cyclin-dependent kinases. In the skin, p53 plays another role in fighting cancers. This is particularly dangerous, since the skin is constantly in a state of replacement from basal cells rising through the epidermis.
Mutation is probably a relatively common occurance.
The result is the peeling of skin that follows sunburn. Thus, peeling skin is a protective mechanism against skin cancer. Sunlight causes skin cancers in two ways. First, it mutagenizes the p53 gene. Second, the heterozygotes produced by the lack one of these gene have a selective advantage over those that have both normal genes.