In this concept of bronchial asthma pathogenesis, the presence of serum allergen-specific immunoglobulin E (IgE) related to atopy/allergy is the hallmark of the adaptive TH2 response, and increased numbers of type 2 cytokine (i.e., interleukin 4 (IL-4), IL5, and IL-13)-producing CD4 positive T cells, which are stimulated by dendritic cells, contribute to eosinophilic airway inflammation and airway hyper-responsiveness (AHR). The gene discussed is IL5; the disease is allergic disease.