In cancer cells, the metabolic abnormalities and oncogenic signaling are always accompanied by the excess ROS accumulation and trigger a redox adaptation response, resulting an increased antioxidant capacity, such as overexpressing of ROS scavengers including Trx and/or GSH and a shift of redox dynamics with exorbitant ROS generation and elimination to keep the ROS levels below the toxic threshold [32,34]. The gene discussed is TXN; the disease is cancer.