At the animal level, RPL39 knockdown significantly decreased the mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) and increased the stroke volume (SV), ejection fraction (EF), and end-systolic volume (Ves) in both male- and female-shRNA groups, compared to male and female PAH groups. This evidence concerns the gene RPL39 and pulmonary arterial hypertension.