Studies confirm that hyperoxia abnormally activates the Wnt/β‐catenin pathway through the NF‐κB‐Wnt5a signaling axis, leading to alveolarization impairment and fibrosis [150], suggesting Wnt5a as a potential therapeutic target for chronic lung diseases including BPD. The gene discussed is NFKB1; the disease is bronchopulmonary dysplasia.