AKT1 and neoplasm: In comparison to normal cells, glucose uptake in tumor cells is enhanced as a consequence of the activity of oncogenes (e.g., those from the PI3K/AKT pathway) that upregulate the cell surface expression of glucose transporter GLUT1 [14], or of the loss of tumor suppressors, such as SIRT6, which leads to increased GLUT1 and GLUT4 expressions and to a reduced carbon flux into mitochondrial respiration (through an increased pyruvate dehydrogenase kinase expression) [15,16,17,18].