AKT1 and cancer: Cancer cells are usually submitted to higher levels of reactive species as a result of aberrations in oxidative metabolism (e.g., impaired mitochondrial oxidative phosphorylation [6] and increased aerobic glycolysis [7]) and signaling pathways (e.g., Ras [8] and AKT [9] activation), which further stimulate the malignant phenotypes of death evasion, angiogenesis, invasiveness, and metastasis [10].