Combined with inflammatory cues, these mutations are thought to suppress BMPR2 (bone morphogenetic protein R2) expression while exacerbating pathological transforming growth factor-β (TGF-β) signaling.4 In patients with PAH, circulating TGF-β1 and activin A levels are elevated.5,6 This imbalance has prompted the exploration of therapeutic strategies targeting the TGF-β pathway, such as sotatercept, and approaches aimed at enhancing BMP9 activity have been explored.7 However, the role of BMP9 in PAH remains controversial. The gene discussed is BMPR2; the disease is pulmonary arterial hypertension.