When allergen stimulates airway epithelial cells that are impaired by asthma or the alveolar macrophages to generate IL-25 and IL-33, ILC2 is induced to proliferate and activate, through binding with corresponding receptors such as IL-25R (also called IL-17RB) and IL33R on the surfaces of ILC2, secreting type 2 cytokines such as IL-13 and IL-5, which promote airway hyperresponsiveness, eosinophilic aggregation, and mucus secretion [7]. The gene discussed is IL13; the disease is airway hyperresponsiveness.