Although Xpa disruption has only received minimal attention in human osteosarcomas, one investigation of polymorphisms in it and other nucleotide excision repair genes found shorter event-free survival from osteosarcoma in cisplatin-treated patients bearing a polymorphism in ERCC2. Similarly, cooperative disruption of p53 and Brca2 generated osteosarcomas in mice, but the increased incidence over baseline was primarily attributed to the former tumor suppressor [77]. The gene discussed is TP53; the disease is neoplasm.