Chemotherapy‐resistant cancer cells exhibit altered redox homeostasis compared to sensitive cells.[87] In particular, resistant lines typically upregulate NRF2‐driven antioxidant defenses to buffer inherently high ROS levels.[88] In our study, the activity of ORP100S, a redox active monothiol TRX variant, is unlikely to have intracellular redox activity as described above and hence might not contribute to ROS defense even in resistant cancers. The gene discussed is TXN; the disease is cancer.