EA patients usually exhibit the secretion of typical Th2 cytokines, such as IL-4, IL-5 and IL-13, and induce Th2 immune response, which then generates a series of cascades downstream, including IgE-stimulated hypersensitivity, airway epithelial cell activation, effector cell (including mast cells, eosinophils and basophils) chemotaxis and epithelial and subepithelial matrix remodeling (10). Here, IL4 is linked to Esophageal atresia.