,72 Another comparative analysis of patients with end-stage lung disease showed distinctive matrisomal phenotypes for end-stage COPD compared with IPF, which had decreased cell-adhesion mediating laminins (laminin subunit beta-1 [LAMB1] and laminin subunit gamma-1 [LAMC1]) and increased collagen VI, suggesting altered adhesion between cells and the ECM as an important aspect of the underlying pathophysiology of IPF.68 This evidence concerns the gene LAMC1 and chronic obstructive pulmonary disease.