For glioblastoma, a highly radioresistant tumor, the combination of the PARP inhibitor E7016 and temozolomide produced a dual DNA damage effect: not only persistently increasing the number of γH2AX foci (P < 0.01) but also significantly extending tumor growth delay by 6 days compared to conventional treatment through the induction of mitotic catastrophe (49). This evidence concerns the gene PARP1 and neoplasm.