Whole genome sequencing of skin cancers arising in XPV−/− patients revealed a strikingly different mutation spectra than that seen in sporadic skin cancer cases (Figure 4A).[34] These XPV−/− tumors not only had significantly elevated mutation densities relative to sporadic skin cancers, but among the mutation classes that were most highly elevated in XPV−/− tumors were T>C, T>A, and especially C>A substitutions. This evidence concerns the gene POLH and skin cancer.