A protective role of BMP9 on inflammation is supported by in vitro and in vivo data showing that BMPRII deficiency causes (1) endothelial inflammation, mediated by reactive oxygen species (ROS) and NFκB, and atherosclerosis (Kim et al., 2013), (2) an exaggerated inflammatory response in human and mouse pulmonary artery smooth muscle cells after lipopolysaccharide (LPS) stimulation, which is associated with increased ROS production (Soon et al., 2015), and (3) LPS-induced pulmonary hypertension in mice (Soon et al., 2015). The gene discussed is BMPR2; the disease is atherosclerosis.