The loss of this protective function in cancer cells treated with ORP100S versus natural thioredoxin likely reflects the existence of multiple TRX‐catalyzed stress‐protective and proliferative signaling pathways, some of which (likely those involving intracellular TRX redox cycling, which is inhibited in ORP100S) are dispensable in non‐cancer cells. The gene discussed is TXN; the disease is cancer.