The quantity and quality of constitutive epidermal melanin determine skin colour and responses to solar ultraviolet radiation (UVR). Epidemiology shows that melanin protects against UVR-induced skin cancer, caused mainly by DNA photodamage, especially the cyclobutane pyrimidine dimer (CPD). Synthesis of vitamin D in the epidermis is the only established benefit of solar UVR exposure, particularly UVB (~295-315nm) radiation. People with higher levels of constitutive melanin have poorer vitamin D status compared with less melanised skin types at given latitude ranges. It is widely assumed that melanin inhibits DNA damage as well as vitamin D synthesis, but we lack quantitative data. One approach to assess the impact of melanin is to compare extreme skin phototypes such as Fitzpatrick skin types II with VI. Such studies show that melanin is highly effective at inhibiting CPD, especially in the basal layer that has a much higher concentration of melanin than the suprabasal epidermis [1]. It was estimated that melanin afforded a protection factor of ~60 in the basal layer that contains keratinocyte stem cells and melanocytes. This level of protection may explain differences in skin cancer incidence in black and white skins. However, comparable studies show that melanin has a very modest inhibitory effect (factor <1.5) on vitamin D synthesis [2]. The most likely reason for large quantitative differences between protection of CPD and inhibition of vitamin D synthesis is the spatial relationship between melanin and photobiological target. In the case of CPD, there is a high concentration of melanin directly above the nuclei of the basal layer cells. In the case of vitamin D, there is sufficient precursor (7-dehydrocholesterol) above the highly melanised basal layer to allow vitamin D synthesis. In summary, it is important to recognise that the effect of melanin depends on endpoint and that blanket statements on melanin are not useful.