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The mutation spectra induced by UVB were investigated by whole\u2010exome sequencing of randomly selected clones of NER\u2010proficient and XP\u2010C\u2010deficient human skin fibroblasts. As a model, a cell line unable to recognize and remove lesions (XP\u2010C) was used and compared to the complemented isogenic control (COMP). As expected, a significant increase of mutagenesis was observed in irradiated XP\u2010C cells, mainly C&gt;T transitions, but also CC&gt;TT and C&gt;A base substitutions. Remarkably, the C&gt;T mutations occur mainly at the second base of dipyrimidine sites in pyrimidine\u2010rich sequence contexts, with 5\u2032T<jats:styled-content>C<\/jats:styled-content>\u2009sequence the most mutated. Although T&gt;N mutations were also significantly increased, they were not directly related to pyrimidine dimers. 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