To increase the specificity and efficacy of NAMPT inhibition, we combined FK866 with β-lapachone (β-lap), a targeted cancer therapeutic that causes tumor-selective PARP1 hyperactivation and NAD+ depletion in an NADPH:quinone oxidoreductase 1 (NQO1)-specific manner.9β-Lap is a substrate for two-electron oxidoreduction by NQO1, a Phase II quinone-detoxifying enzyme.9 The resulting hydroquinone form of β-lap is highly unstable and spontaneously reacts with oxygen to revert back to the parent compound, generating two moles of superoxide per mole of NAD(P)H used in the process. The gene discussed is PARP1; the disease is cancer.