Such techniques have revealed dysregulation of endothelial nitric oxide synthase (eNOS) in cell culture models of PAH; siRNA-mediated knockdown of BMPR2 induced endothelial dysfunction in human PAECs, caused by a reduction in BMP2/4-mediated production of the vasodilator nitric oxide by eNOS [127]. Here, BMPR2 is linked to pulmonary arterial hypertension.