While it has been previously proposed that thickening of the airway RBM may lead to defective cross-talk in the epithelial-mesenchymal trophic unit leading to increased inflammation and fibrosis, the data reported in this study highlight that increased deposition of fibronectin and fibrillar collagen-I could potentially be beneficial and enhance attachment of the damaged and defective airway epithelium observed in patients with asthma (41, 50, 51). This evidence concerns the gene FN1 and asthma.