The clinical syndrome of bronchopulmonary dysplasia (BPD) in preterm infants results primarily from an arrest of lung vascular and alveolar development. The most likely mediators are proinflammatory cytokines that are induced by antenatal exposure to infection, postnatal ventilation, and oxygen exposure. New epidemiologic data suggest that attempts to avoid intubation and ventilation are the best ways to avoid severe BPD. The claim that one ventilation technique is better than another remains unconvincing, and any strategy that maintains the lung open and minimizes tidal volumes probably will be helpful. More adverse effects of postnatal steroids are being recognized. New insights into the pathophysiology of BPD and a new emphasis on minimizing ventilation and ventilator-mediated injury should improve outcomes for very preterm infants.