The explanation for this discrepancy can be found in recent papers showing that some cancer cell lines—including HCT116—are not affected by L-BSO or GSH synthesis inactivation because they can compensate GSH depletion by the thioredoxin (TXN) pathway25, and by maintaining protein homeostasis through deubiquitinating enzymes (DUB)32. The gene discussed is TXN; the disease is cancer.