Relatedly, activated β-catenin has been shown to be up-regulated in the nuclei of myofibroblasts of fibroblastic foci of IPF patients [14], and alveolar epithelial responses to TGF-β involve alpha3 integrin for β-catenin phosphorylation and formation of a β-catenin/p-Smad2 complex resulting in initiation of EMT [31]. Here, SMAD2 is linked to idiopathic pulmonary fibrosis.