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 hypertension.