Like in asthma, Th2 cells intensively responded to allergens, its excess secretion IL-4, IL-13 promoted recruitment of eosinophils to pulmonary or/and bronchial surface, and subsequent CCL24 produced by eosinophils enhanced above process [20]; similar acceleration of CCL24 by IL-13 stimulation could be found in oesophageal in vitro experiment [10]. The gene discussed is CCL24; the disease is asthma.