For example, ROS promote the survival of tumor cells by activating mitogen activated-protein kinase (MAPK)/extracellular-regulated kinase 1/2 (ERK1/2) [31], phosphoinositide-3-kinase (PI3K)/Akt [32] and nuclear factor-κB (NF-κB) pathways [33], inactivating the tumor-suppressor gene p53 [34] and stabilizing the transcriptional factor Nrf2 [35]. The gene discussed is AKT1; the disease is neoplasm.