Our results implied increased fatty acid metabolism due to increased expression of genes for beta oxidation, such as Acyl-CoA dehydrogenases isoforms M (ACADM) and Acetyl–Coa Acetyl transferase1 (ACAT1), suggest that fatty acid metabolism may play an important role in human PAH by switching the fuel of existing mitochondrial oxidative metabolism from glucose to fatty acids. The gene discussed is ACAT1; the disease is pulmonary arterial hypertension.