Evidence for glycolysis contributing to the development of PAH comes in part from the observation that pharmacologic or genetic inhibition of the positive glycolytic regulator PFKFB3 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3) ameliorates the development of pulmonary hypertension in animal models [25]. This evidence concerns the gene PFKFB3 and pulmonary arterial hypertension.