Asthma is accompanied by the thickening of the basement membrane due to the excessive production of matrix proteins typically synthesized by fibroblasts and myofibroblasts, including collagen I and III as well as fibronectin-EDA and tenascin C. Our results shown above suggested that bronchial epithelial cells can transition into a mesenchymal-like phenotype upon TGFβ1treatment and might therefore contribute to deposition of excessive matrix proteins. The gene discussed is FN1; the disease is asthma.