To increase the specificity and efficacy of GLS1 inhibition in PDA, we combined BPTES or CB-839 with ß-lapachone (ß-lap), a targeted cancer therapeutic that causes tumor-selective reactive oxygen species (ROS) formation in an NADPH:quinone oxidoreductase 1 (NQO1)-specific manner [18]. This evidence concerns the gene GLS and Patent ductus arteriosus.