Biochemical evidence reveals that Gq signaling is central in the pathophysiology of PAH as the endothelin 1 (ET-1) system is upregulated (Stewart et al, 1991), serotonin (5-HT) activity enhanced (Hervé et al, 1995) and thromboxane metabolite levels are increased in PAH patients (Christman et al, 1992), likewise, antagonists of GPCRs activating Gq are also of therapeutic relevance (Rubin et al, 2002). The gene discussed is EDN1; the disease is pulmonary arterial hypertension.