We hypothesize that KP372-1 is a better drug candidate than β-lap because NQO1-dependent redox cycling of KP372-1, as a single agent or combined with clinically relevant PARP inhibitors (PARPi), creates deleterious DNA lesions at a much lower dose, initiates DNA damage response, promotes cell death and offers a promising strategy to target pancreatic cancer. The gene discussed is PARP1; the disease is familial pancreatic carcinoma.