Wnt/β‐catenin has been shown to increase proliferation of lung epithelial cells during lung epithelial injury and repair.4 Furthermore, Wnt3a activation can inhibit neutrophils influx into the alveolar airspace of injured lungs as well as experimental emphysema.5 However, the molecular mechanisms underlying the protection of Wnt signal against COPD are unknown. The gene discussed is WNT3A; the disease is chronic obstructive pulmonary disease.