To address this question, we used two different endothelial models carrying heterozygous LOF ALK1 mutations: (1) endothelial colony-forming cells (ECFCs) that were isolated from the cord blood of newborns with an HHT-affected parent and (2) Human microvascular endothelial cells (HMVECs) isolated from explanted lungs of PAH patients. The gene discussed is ACVRL1; the disease is pulmonary arterial hypertension.