The multifactorial, “multihit” model of PAH pathogenesis converges on a persistently dysregulated, pro-proliferative, anti-apoptotic, and pro-fibrotic vascular phenotype sustained by an imbalance within the transforming growth factor β (TGF-β) superfamily and by interlinked inflammatory–metabolic crosstalk [7,59,60]. Here, TGFB1 is linked to pulmonary arterial hypertension.