GSTO2 (glutathione S-transferase omega 2) is a cytoplasmic oxidoreductase that exhibits glutathione-dependent thiol transferase activity and high dehydroascorbate reductase activity, contributing to ascorbic acid recycling and xenobiotic biotransformation including arsenic metabolism 1. In cellular stress responses, GSTO2 protects against oxidative injury and ferroptosis; in intracerebral hemorrhage models, GSTO2 upregulation ameliorates neuronal apoptosis, inflammation, ferroptosis, and oxidative stress by increasing GPX4 expression 2. However, GSTO2 expression is frequently lost in lung squamous cell carcinoma through DNA hypermethylation, and forced GSTO2 expression inhibits cancer cell growth and metastasis via p38/β-catenin signaling 3. Genetically, GSTO2 polymorphisms carry disease relevance: the rs156697 variant's GG genotype increases asthma risk (OR 5.91) 4 and NSCLC risk by promoting the full-length GSTO2-V1 isoform over the growth-inhibitory truncated GSTO2-V2 variant 1. The GSTO2*D142 variant also associates with allergic diseases 5 and glaucoma when combined with GSTO1 variants 6. These findings establish GSTO2 as a context-dependent regulator with protective roles in neurodegeneration but tumor-suppressive functions in lung cancer.