In our study, we found that exposure of NQO1+ cancer cells to KP372-1 alone caused PARP1 hyperactivation and NAD+/ATP depletion, and cells underwent autophagy and capase-7 dependent apoptosis, while exposure of these cells to KP372-1 + PARP inhibitor rucaparib induced elevated ROS formation and inhibition of DNA repair resulting in rapidly autophagic and apoptotic cell death (Figures 2G, H, 4E, 5B–E, and Figures S2E–G). Here, PARP1 is linked to cancer.