The molecular and cellular mechanisms involved in the pathogenesis of PAH are complex and involve cross-talk between several signalling pathways including the transforming growth factor beta (TGF-β)/bone morphogenetic protein (BMP) axis8, growth factors (e.g. PDGF)9 and vasoactive proteins (e.g. vasoactive intestinal peptide (VIP)10 and endothelin-1 (ET-1)11 (reviewed with respect to anti-remodelling therapies in ref. 5). The gene discussed is VIP; the disease is pulmonary arterial hypertension.