Ultraviolet (UV) radiation is a very common carcinogen in our environment. Epidemiological data on the relationship between skin cancers and ambient solar UV radiation are very limited. Hairless mice provide the possibility to study the process of UV carcinogenesis in more detail. Experiments with this animal model have yielded quantitative data on how tumor development depends on dose, time and wavelength of the UV radiation. In addition, at the molecular level the interactions between UV, specific cancer genes-like the Ras oncogene family and the p53 tumor suppressor gene, together with the role of DNA repair in this process have been addressed recently. In wildtype hairless mice mutations in the p53 gene are clearly linked to UVB but not to UVA radiation. Furthermore, the p53 alterations seem to be essential early in tumor development. However, in Xpa-deficient mice this dependency on p53 alterations appeared to be different as is the tumor type induced by UVB. Research using genetically modified hairless mice should enable us to further unravel the mechanisms of UV-induced skin cancer.