TRAIL has been found to be increased within pulmonary vascular lesions of patients with pulmonary hypertension (206) and also in a mouse model of hypoxia-induced pulmonary hypertension, levels of soluble TRAIL correlated with right ventricular systolic pressure, right ventricular hypertrophy, and pathologic alterations (33, 34). This evidence concerns the gene TNFSF10 and pulmonary arterial hypertension.