,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 Here, LAMC1 is linked to idiopathic pulmonary fibrosis.