Several studies have demonstrated that altered glycolysis in HNSCC is associated with the activation of hypoxia-inducible factor-1 (HIF-1), transketolase-like protein 1 (TKTL1), mutations in tumor suppressor gene p53, and overexpression of the glucose transporters-1 (GLUT-1) [32]. The gene discussed is TP53; the disease is head and neck squamous cell carcinoma.