Analogously, mice deficient in IL-4 fail to develop AAD in response to most allergens and immunization protocols [13, 14]; airway inoculation with IL-4 or IL-13 (or genetic overexpression of either cytokine) can induce airway eosinophilia, goblet cell metaplasia and AHR [15–17]; and treatment with antagonists of IL-13 or IL-4Rα can usually suppress established AHR [18–21]. The gene discussed is IL4R; the disease is Increased total eosinophil count.