PFKM and neoplasm: Tumor cells exploit several strategies to inhibit rate-limiting glycolytic enzymes: pyruvate formation is controlled by enhanced expression of the pyruvate kinase enzyme M2 (PKM2) [15]; phosphofructokinase 1 (PFK1) is inhibited either by induction of the fructose-2,6-bisphosphatase TP53-inducible glycolysis and apoptosis regulator TIGAR [16], or by increasing intracellular levels of citrate, a PFK1 allosteric inhibitor [17].