In terms of fibroblasts, which are an important producer of ECM within the lamina propria, Ong and colleagues showed that parenchymal lung fibroblasts of COPD patients overexpress miR-455-3p and miR-21-3p, compared to controls, when stimulated by TGF-β, resulting in the induction of fibronectin and collagen I through the TGF-β and wnt (wingless and Int-1) signalling pathways [131]. The gene discussed is FN1; the disease is chronic obstructive pulmonary disease.