The model of OVA-induced allergic asthma used in this study is characterized by T helper 2 cell release of cytokines such as IL-4, IL-5, and IL-13, as well as the eosinophil chemoattractant eotaxin, which contribute to airway inflammation in asthma [23, 24] Among other functions, these cytokines induce fibroblast proliferation, extracellular matrix deposition, airway hyperresponsiveness, epithelial cell apoptosis, mucus production, and eosinophil recruitment [31]. The gene discussed is IL4; the disease is asthma.