By combining NAMPT inhibitors (e.g., FK866) and NQO1 bioactivatable drugs (e.g., β-lap, ARQ761) we exploit the reliance of PDA on rapid NAD+ synthesis, as well as the tumor-selective overexpression of NQO1 through the use of agents that are bioactivated to induce cell death. The gene discussed is NQO1; the disease is neoplasm.