Previous studies have pointed out human pulmonary vascular cells sense type I IFN readily in the circulation and would release interferon γ inducible protein 10 (IP10) and endothelin-1 (ET-1) under the stimuli of high IFNα (20), which both play as key mediator in the pathogenesis of PAH (21, 22). The gene discussed is EDN1; the disease is pulmonary arterial hypertension.