If postnatal HIF2α activity despite high environmental oxygen levels is actually key for the correct alveolarization of the lung, this might explain why PHD inhibition ameliorates the lung hypoplasia observed in mouse models of hyperoxia-induced lung injury [37, 38] or in primate models of bronchopulmonary dysplasia [39, 40]. The gene discussed is PDC; the disease is bronchopulmonary dysplasia.