This enzyme was selected because as we have recently shown, it is increased in IPF where it may play a profibrotic role increasing the proliferative and migratory phenotype of epithelial cells in a catalytic dependent manner.[18] Likewise, increased expression and release of MMP28 has been reported in hypertrophic scars.[28] Importantly, there is some evidence suggesting that MMP28 induces a coordinated TGF-β-dependent program leading to epithelial to mesenchymal transition, a biological process that has been implicated in the pathogenesis of IPF.[2, 18, 29]. This evidence concerns the gene TGFB1 and idiopathic interstitial pneumonia.