On the parenchymal level, HIF-2α may play a different role, as recently revealed by Pasupnetiet al. [50]: human emphysema lung ECs expressed reduced HIF-2α levels and EC-specific deletion of Hif-2α in the mouse model led to emphysema development, whereas its overexpression prevented emphysema after SU5416 exposure. The gene discussed is EPAS1; the disease is pulmonary emphysema.