Primarily, the “synthetic lethality” induced by exogen blockade of base excision repair (BER) machinery, used by tumor cells to escape the HRR defect; the PARPi binds and “traps” PARP-1 enzyme on the chromatin, creating a damage necessitating HRR for its removal, and the enhancement of non-homologous end joining, which may elicit a tumoricidal effect [13]. Here, PARP1 is linked to neoplasm.