Importantly, sequestration of activin-class ligands with an Fc-fusion protein incorporating the extracellular domain of activin receptor type IIA (ActRIIA-Fc) exerts antiproliferative and inflammation-suppressing effects in the lung vasculature, reverses pulmonary vascular remodeling, and reduces PH in experimental PAH, thus exhibiting disease-modifying activity not observed with vasodilator-based therapy (15, 16). This evidence concerns the gene ACVR2A and pulmonary arterial hypertension.