By combining GLS1 inhibition (e.g., CB-839) and NQO1-bioactivatable drugs (e.g., β-lap, ARQ761), we exploit the reliance of PDA on glutamine for redox balance, as well as the tumor-selective overexpression of NQO1 through the use of a unique agent that is bioactivated to induce cell death. Here, GLS is linked to neoplasm.