In chronic hypoxia–induced PAH mouse models, myeloid cell–specific deletion of HIF-1α reduces pulmonary macrophage infiltration and markedly attenuates vascular remodeling and PAH phenotypes, suggesting that macrophage HIF-1α plays a pro-pathogenic role in hypoxia-driven vascular pathology (74). The gene discussed is HIF1A; the disease is pulmonary arterial hypertension.