Further research has shown that the lack of protective effects from BMPRII signaling along with increased inflammatory activity (facilitated by cytokines like IL‐6) may be a major factor promoting vascular remodeling of smooth muscle and endothelial cells of the pulmonary vasculature in PAH (Hagen et al., 2007; Hiepen et al., 2019; Steiner et al., 2009). The gene discussed is BMPR2; the disease is pulmonary arterial hypertension.