Apart from being as a general tumor suppressor gene, p53 also plays an important part in regulating of metabolism. p53 activates hexokinase 2 (HK2) that converts glucose to glucose-6-phosphate (G6P) which enters glycolysis to produce ATP, or enters the pentose phosphate pathway (PPP). It therefore, supports macromolecular biosynthesis by producing reducing potential in the form of reduced Nicotinamide adenine dinucleotide phosphate (NADPH) and/or ribose that are used for nucleotide synthesis. p53 inhibits the glycolytic pathway by upregulating the expression of TP53-induced glycolysis and apoptosis regulator. Wild-type p53 supports the expression of PTEN (gene), which inhibits the PI3K pathway, thereby suppressing glycolysis. POU2F1 also cooperate with p53 in regulating the balance between oxidative and glycolytic metabolism. It provides resistance to oxidative stress that would regulates a set of genes that increase glucose metabolism and reduce mitochondrial respiration. This will provide additive force when the p53 is lost. Mutated Ras also enhances glycolysis, partly through increasing the activity of Myc and hypoxia-inducible factors. Although HIF-1 inhibits Myc, HIF-2 activates Myc causing the multiplicity of the tumor cells.