Complementation studies from fibroblasts derived from XP patients have shed light on the fundamental players involved in this pathway: mutations in seven different NER genes [from Xeroderma pigmentosum, complementation group A (XPA) to Xeroderma pigmentosum, complementation group G (XPG); De Weerd-Kastelein et al., 1972] plus a variant form, Xeroderma pigmentosum, complementation group V (XPV), defective in the translesion DNA polymerase eta (Lehmann et al., 1975), lead to XP. The gene discussed is ERCC5; the disease is xeroderma pigmentosum.