Nucleotide excision repair (NER) is a process by which cells identify and repair DNA lesions resulting from chemical or radiation exposure (1). XPC forms a complex with HR23B (2) that acts as a damage sensor due to its high affinity for geometry distorting DNA lesions. This complex localizes to sites of DNA damage and recruits the remaining members of the preincision complex necessary for initiation of NER (3). XPC is one of eight NER proteins (XPA-G, XPV) where defects result in Xeroderma pigmentosum, a disease characterized by sunlight sensitivity, a predisposition to cancer of exposed tissue, and, in some instances, neurological defects (4).