The role of TLS in preventing cancer is clearly demonstrated in the sun-sensitive skin cancer-prone disease xeroderma pigmentosum variant (XP-V), where the absence of Pol η as a result of inactivating mutations in POLH (147, 148) leads to prolonged replication arrest at the sites of UV-induced lesions in the template. The gene discussed is POLH; the disease is Xeroderma pigmentosum variant.