Both human and animal data coming largely from Vanderbilt [120,122,123,124], Glasgow [119,125,126], and Penn State Universities [14,127] clearly point toward a pathogenic role for CYP1B1 with regard to the risk of PAH in humans and toward a pathogenic 16αHE1–BMPR2 interaction in experimental PH. The gene discussed is CYP1B1; the disease is pulmonary arterial hypertension.