[47] suggest that FBLN1 may be involved in the pathogenesis of not only COPD but also of asthma and IPF. Specifically, [47] show that the deletion of FBLN1’s variant FBLN1C in mouse models inhibits airway and lung remodeling in chronic asthma and lung fibrosis while also protects against COPD. The FBLN1C variant is known to increase the proliferation of lung fibroblasts in COPD and IPF patients [48]. This evidence concerns the gene FBLN1 and chronic obstructive pulmonary disease.