AKT1 and cancer: High ROS production in cancer can result in the inactivation of H2O2 scavenger enzymes like glutathione peroxidase (GPX), glutathione reductase (GRX), catalase (CAT), superoxide dismutase (SOD), superoxide reductase, thyroxine (TRX), and peroxiredoxin (PRX) and the tumor suppressor gene phosphatase and tensin homolog (PTEN), a negative regulator of the PI3K/AKT signaling pathway, as well as the oxidation and inactivation of many other protein tyrosine phosphatases (PTPs) such as tyrosine-protein phosphatase non-receptor type 1 (PTP1B) [89].