We now know that in patients with PAH, pulmonary arterial endothelial TPH1 expression is increased and that endothelial-derived serotonin can act on the underlying pulmonary arterial smooth muscle cells (PASMCs) in a paracrine fashion.9 Recently, this has been shown to be facilitated by myoendothelial gap junctions.10 Endothelial TPH1 expression is also increased in animal models of PH.11 Pathologically, PAH is characterized by vasoconstriction of the small pulmonary arteries and proliferation in all layers of the vessel wall as well as fibrosis and inflammation. Here, TPH1 is linked to pulmonary arterial hypertension.