It has been found that the inactivation of AMPKα promotes a metabolic shift to aerobic glycolysis and that these metabolic effects require HIF-1α to maintain stability, as silencing HIF-1α reverses the shift to aerobic glycolysis and the biosynthetic and proliferative advantages of reduced AMPKα signaling in tumor cells (51). The gene discussed is HIF1A; the disease is neoplasm.