Studying the effects of hyperoxia on AT2 cells over time revealed increased β-catenin and WNT5a signaling, which mirrors elevated WNT5a signaling in lung tissue from infants with BPD, and led to the discovery that a WNT5a inhibitor abrogates some of the effects of hyperoxia in precision cut lung slices. The gene discussed is WNT5A; the disease is bronchopulmonary dysplasia.