Tumor suppressors, such as PTEN or LKB1, inhibit oncogenic signaling, which are central activators of glycolysis (Akt, AMPK, HIF and p53), and undergo hypermethylation of their promoters, facilitating the activation of glycolysis and the synthesis of macromolecules, thus helping to maintain the glycolytic phenotype [21,90]. The gene discussed is TP53; the disease is neoplasm.