Having found that the combination of SERCA2a/BMPR2 and SERCA2a/STAT3i inhibited pulmonary vascular cell proliferation and restored BMPR2 in vitro, we evaluated and compared the effects of AAV1.hSERCA2a/AAV1.hBMPR2 and AAV1.hSERCA2a/STAT3i in vivo on pulmonary hemodynamics and vascular remodeling in the severe PAH model induced by unilateral left pneumonectomy combined with monocrotaline (PNT/MCT). Here, BMPR2 is linked to pulmonary arterial hypertension.