Considering that the mechanism of BTZ cytotoxicity often involves induction of ROS in sensitive cancer cells (17) and that Onc-p53 might alter the tumor cell oxidative state (15), we mined the metabolomic profiles of 52 human NSCLC cell lines that included those expressing Onc-p53 alleles versus those exhibiting p53 loss-of-function (homozygous deletion, frameshift, and early termination alleles associated with loss of heterozygosity) for abundance of the key antioxidant metabolite GSH [both reduced (GSH) and oxidized species (GSSH) of GSH; ref. 20]. This evidence concerns the gene TP53 and cancer.