The rationale for platelet-derived growth factor involvement in the pathogenesis of PAH is strong, with increased expression of ligand and phosphorylated receptor in patient lung tissue.44 However, we did not observe any change in the platelet-derived growth factor subunit B (homodimer) levels in the spent culture medium from serotonin-stimulated control and PAH-hPASMCs. This evidence concerns the gene PDGFB and pulmonary arterial hypertension.