As previously reviewed in depth by Boucherat et al. [3], serotonin (5-HT) and thromboxane A2 (TXA)—as well as other endogenous small molecules including endothelin-1 (ET-1) and platelet-derived growth factor (PDGF)—have been shown to negatively regulate Kv expression and function in PAH models. The gene discussed is EDN1; the disease is pulmonary arterial hypertension.