It is a widely documented fact that the deposition of different ECM components, including collagen types I, III and V, fibronectin, tenascin and proteoglycans (lumican and biglycan) is increased during IPF, COPD and ARDS [90,91], and in turn, the main effector cells responsible for the increased production of ECM proteins, are fibroblasts [92,93] and the airways’ smooth muscle cells, the proliferation of which is a key characteristic of the airways in patients with pulmonary fibrosis and COPD [94,95]. This evidence concerns the gene FN1 and chronic obstructive pulmonary disease.