Among them, PKM2 tetramer increases glycolytic flux and promotes high ATP production, whereas dimeric PKM2 not only directly promotes aerobic glycolysis by redirecting glucose-generated carbon to biogenic enzymes, but also translocases to the nucleus and acts as a protein kinase to phosphorylate histone H3 and activate the transcription of various genes such as c-MYC and STAT3, which indirectly supports aerobic glycolysis and promoting the progression of tumor cell proliferation [60–63]. The gene discussed is PKM; the disease is neoplasm.