These results are in agreement with an experimental lung fibrosis study which confirmed that the constitutive and/or inducible transgenic overexpression of IL-13 in the murine lung induces airway inflammation involving macrophages, lymphocytes and eosinophils, airway remodeling with subepithelial fibrosis, parenchymal fibrosis, mucus metaplasia, and striking increases in alveolar size, lung size, and pulmonary compliance [37]. The gene discussed is IL13; the disease is pulmonary fibrosis.