Specifically, the cancer phenotypes could arise when XPB-dependent DNA repair defects alter hyperproliferative input(s); e.g., defective function of the FUBP1/FIR/TFIIH nexus would be predicted to disrupt repression of the MYC oncogene and contribute to XP-related neoplasia. The gene discussed is MYC; the disease is xeroderma pigmentosum.