Interestingly, we showed that when PARP-1KO mice were crossed with Ptch1+/− mice, a cancer prone mouse model in which induction of DNA damage accelerates development of cerebellum and skin malignancies, double mutants further accelerated medulloblastoma (MB) and basal cell carcinoma development following irradiation, providing evidence that PARP-1 function suppresses Ptch1-associated tumors arising in response to environmental stress [85]. The gene discussed is PTCH1; the disease is cancer.