In particular, bosentan seems to be able to suppress the ET-1-induced production of TNF-α and other proinflammatory mediators by monocytes in vitro [11]. In vivo, bosentan significantly reduces IL-6, ICAM-1, and pro-brain natriuretic peptide (pro-BNP) serum levels in patients with PAH [40] and leads to the normalization of soluble adhesion molecules in SSc-associated PAH [40, 41]. The gene discussed is TNF; the disease is pulmonary arterial hypertension.