Furthermore, inactivation of p53 in tumor cells shifts metabolism from mitochondrial respiration towards glycolysis including overexpression of glucose trasporters GLUT1, GLUT4 and GLUT3, enhancement of the expression of glycolytic enzymes such as phosphofructokinase and phosphoglycerate mutase, suppression of mitochondrial respiration by inhibiting the synthesis of cytochrome c oxidase 2 and activation of AKT and HIF, which are effectors of downstream of PI3K [36,37]. Here, TP53 is linked to neoplasm.