Most XP patients have mutations in XPA through XPG, and XPV (also named POLH), mainly involved in nucleotide excision repair of ultraviolet (UV) irradiation.[6–8] Classical XP phenotypes include acute sunburn, persistent erythema on minimal sun exposure, noticeable freckles, photophobia, keratitis, skin lesions on lids, and even nervous abnormities, while patients carrying POLH variants, slightly affected in general, might only have accumulated UV-induced lesions like xerosis and poikiloderma limited to sun-exposure sites. The gene discussed is XPA; the disease is keratitis.