Yu et al. [85] revealed that Cav1F92A-modified rat bone marrow mesenchymal stem cells (rBMSCs/Cav1 F92A) activate the NO/cGMP pathway, inhibit TNF-α, TGF-β1, thrombospondin-1, and MGP expression, and consequently suppress cell migration in monocrotaline-treated human pulmonary artery smooth muscle cells (HPASMCs), suggesting that rBMSCs/Cav1 F92A might represent a therapeutic approach for pulmonary hypertension, which functions by inhibiting the switching of HPASMCs from a contractile to synthetic phenotype. This evidence concerns the gene CAV1 and pulmonary arterial hypertension.