In addition, they also found that the effects of BMPR2 regulation on non-SMAD signaling increased phosphoinositide-3 kinase, reduced phosphorylated-p38-mitogen-activated protein kinase, and upregulated nitric oxide production in the microvascular endothelial cells, which were related to relief of PAH, such as the decrease in right ventricular, mean pulmonary artery pressure and Fulton Index (Feng et al., 2016; Harper et al., 2016). The gene discussed is BMPR2; the disease is pulmonary arterial hypertension.