Our results conclusively evidence that POMHEX treatment renders ENO1 deleted gliomas substrate limited for mitochondrial respiration, and supplementation of pyruvate mitigates POMHEX toxicity by restoring mitochondrial respiration and ATP production and only minimally by NAD+/NADH redox shift and stimulation of glycolysis (Supplemental Figure S5, S6, S7). This evidence concerns the gene ENO1 and central nervous system cancer.