We hypothesize that treatment with a PARPi rucaparib (FDA approved) prior to exposure to KP372-1 will enhance both drugs antitumor effects through KP372-1-induction of superoxidase and hyperactivation of AKT and PARPi’s inhibition of PARP-driven DNA repair in a tumor-selective manner and thereby overcome a major PARPi resistance mechanism. The gene discussed is PARP1; the disease is neoplasm.