One of the ways hyperactivation of the PI3K/AKT/mTOR pathway is achieved in various tumor types [169] is by the ROS‐mediated oxidation of key cysteine residues in negative regulators (phosphatase and tensin homolog (PTEN) and protein tyrosine phosphatase 1b (PTP1b)), which renders both proteins inactive [170, 171]. This evidence concerns the gene PTPN1 and neoplasm.