However, the cytotoxicity and efficacy of PARPi currently used in clinic or in ongoing clinical trials, including niraparib, rucaparib, talazoparib, olaparib, and veliparib, in contrast with their abilities of PARP activity inhibition and trapping, seem to have a much broader range (4, 5) of functions, which raises the important questions of whether there exist other molecular mechanisms of PARPi function in tumor cells and how to increase the sensitivity of cancer to PARPi. This evidence concerns the gene PARP1 and neoplasm.