The pro-inflammatory phenotype of pulmonary endothelial cells in PAH is characterized by increased surface expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, and accompanied by an excessive release of cytokines and chemokines (3). Here, VCAM1 is linked to pulmonary arterial hypertension.