The decrease in transpulmonary ICAM-1 and VCAM-1 concentrations in PAH children (fold change 0.86 and 0.85, respectively; Figures 3A,B) indicates either intrapulmonary uptake or increased intrapulmonary degradation of these vascular injury mediators that drive endothelial dysfunction (1, 2). The gene discussed is ICAM1; the disease is pulmonary arterial hypertension.