The imbalance of the CD39/ATP axis leads to excessive activation of downstream NLRP3 inflammasome, releases a large number of pro-inflammatory factors such as IL-1β and IL-18, aggravates the polarization of Th2 and Th17 cells, and ultimately promotes airway inflammation and airway hyperresponsiveness in asthma. This evidence concerns the gene IL1B and airway hyperresponsiveness.