Using both mutant (bmpr2R899X+/-) and wild-type (bmpr2+/+) mouse PASMCs in an MTT assay, we observed that the bmpr2R899X mutation—previously linked to the hyperproliferative phenotype of PAH—exhibited enhanced proliferation upon TGF-β stimulation, consistent with earlier reports [69,70,71]. This evidence concerns the gene BMPR2 and pulmonary arterial hypertension.