Summary The development of actinic keratosis (AK) and squamous cell carcinoma (SCC) is the result of a complex sequence of events initiated by exposure to ultraviolet (UV) light. The application of sunscreens prior to sun exposure has been reported to reduce the incidence of AK. The initial damage takes place in the DNA and most of the UV‐induced lesions in the DNA are repaired. However, mutations may occur as a result of base mispairing of the cell and its DNA replicate before the DNA lesion is repaired. The genes involved in the repair process are also potential UV targets. Mutations in the tumour suppressor gene p53 are a common feature of AK and SCC. The hairless mouse is the best available animal model, in which lesions resembling human AK (papillomas), keratoacanthomas and SCCs may be induced. This model of multistage carcinogenesis offers an excellent tool for mechanistic studies. The relative efficacy of UV wavelengths (action spectrum) that induce SCC has been determined using the hairless mouse as a model. The action spectrum has been extrapolated to humans skin and is recognised worldwide.