Hypoxia alone or in combination with other vascular stresses contributes to PAH pathology1 and RhoB can be activated by numerous other factors implicated in the pathogenesis of PAH, including tyrosine kinases TGF-β/bone morphogenetic protein/smad pathway and growth factors, fibroblast growth factor, epidermal growth factor, and PDGF.3 The gene discussed is TGFB1; the disease is pulmonary arterial hypertension.