Acetylation of PKM2, which is dependent upon acetyl-CoA (which is derived from some of the pyruvate in mitochondria that is not converted to lactate) availability, may promote PKM2 degradation and may lead to an increased flux through anabolic synthesis pathways [6], suggesting that PKM2 acts as a glycolytic switch that can be rapidly inactivated in tumor cells by several mechanisms. The gene discussed is PKM; the disease is neoplasm.