Idiopathic pulmonary fibrosis (IPF) is characterized by progressive (myo)fibroblast accumulation and collagen deposition. One possible source of (myo)fibroblasts is epithelial cells that undergo epithelial-mesenchymal transition (EMT), a process frequently mediated by TGF-beta. In this issue of the JCI, Kim et al. report that epithelial cell-specific deletion of alpha3 integrin prevents EMT in mice, thereby protecting against bleomycin-induced fibrosis (see the related article beginning on page 213). The authors propose a novel mechanism linking TGF-beta and beta-catenin signaling in EMT through integrin-dependent association of tyrosine-phosphorylated beta-catenin and pSmad2 and suggest targeted disruption of this interaction as a potential therapeutic approach.