These metabolic findings are consistent with previous reports of decreased PDH activity and increased reliance on glycolysis in RV in PAH [6] Based on the therapeutic benefits of reactivating PDH using the PDK inhibitor dichloroacetate, this pathway accounts for much of the impairment of mitochondrial function in RVF-PAH [24]. The gene discussed is PDP1; the disease is pulmonary arterial hypertension.