Diminished BMPR2 signaling, combined with excess GDF ligands (including GDF8 and GDF11), is thought to promote pulmonary vascular remodeling in PAH by disrupting the normal balance of antiproliferative and pro-proliferative signaling that regulates the growth of pulmonary vascular smooth muscle and endothelial cells34,35. Here, GDF11 is linked to pulmonary arterial hypertension.