The glycolytic switch is thought to be driven by the hypoxic tumor microenvironment through HIF-1α activation, aberrant signaling due to oncogene activation (e.g., Ras, PI3K/mTOR, c-Myc), tumor suppressor gene inactivation (e.g., p53), or by mutations in the OXPHOS pathway [47, 48]. This evidence concerns the gene TP53 and neoplasm.