GSTT2 encodes a theta-class glutathione S-transferase that catalyzes conjugation of reduced glutathione to hydrophobic electrophiles and possesses sulfatase activity. The gene is located on chromosome 22.2 and exists in two forms: a functional gene and a pseudogene (GSTT2P) that arose through duplication with splice-site abnormalities. GSTT2-2 demonstrates activity against diverse substrates including cumene hydroperoxide and lipid peroxidation products, suggesting a protective role against oxidative stress 1. In cancer biology, GSTT2 expression patterns correlate with clinical outcomes. Loss of GSTT2 expression is associated with improved response to BCG immunotherapy in non-muscle-invasive bladder cancer patients, mediated through reduced immunosuppressive PD-L1 expression and enhanced M1 macrophage infiltration 2. Conversely, elevated GSTT2 in pancreatic ductal adenocarcinoma drives resistance to arsenic trioxide by inhibiting ferroptosis through the NRF2-GSTT2-GPX4 axis; GSTT2 silencing restores drug sensitivity 3. In colorectal and esophageal tissues, polyphenol metabolites upregulate GSTT2 expression, enhancing protection against genotoxicity 4 5. These findings identify GSTT2 modulation as a potential therapeutic strategy, particularly checkpoint inhibition in bladder cancer or ferroptosis induction in pancreatic cancer.