These included the activation of protease‐activated receptor 2, the EGFR pathway, adenosine triphosphate and purinergic receptor‐dependent release of IL33, and oxidative stress, which drove mucin expression and goblet cell metaplasia, Th2 cytokine production, reduced barrier integrity, eosinophil recruitment, and airway hyperresponsiveness. This evidence concerns the gene MUC5AC and airway hyperresponsiveness.