Based on the hypothesis that the loss of endothelial BMPRII and circulating BMP9 could be rescued by supplementation of BMP9, it was reported in 2015 that administration of recombinant BMP9 reversed PAH in three different rodent models: a genetic mouse knock-in model containing a human BMPR2 mutation, the monocrotaline (MCT) — induced rat model, and a rat model induced by Sugen alongside chronic hypoxia (Sugen-Hypoxia) [22]. This evidence concerns the gene GDF2 and pulmonary arterial hypertension.