Cells from most patients with xeroderma pigmentosum (XP) can be shown to be defective in repairing ultraviolet (UV) light-induced damage to their DNA, for they have a reduced rate of UV-induced thymidine incorporation. XP variants, however, have clinical manifestations of XP, but all their tissues tested to date have a normal rate of UV-induced 3H-thymidine incorporation. We have now tested tumor cells from an XP variant and from a typical XP patient. The variant's tumor cells, in contrast to those of the typical patient, had no detectable defect in their UV-induced thymidine corporation. We conclude, therefore, that the cells that formed tumors in this XP variant resemble his other cells in DNA repair capacity, and do not represent a minor cell population with the kind of DNA repair defect that is reflected in reduced UV-induced thymidine incorporation.