1992; Okamoto et al. 1998). There is evidence that alterations of Cav-1 function lead to ECM production in fibroblasts and are associated with lung fibrosis (Wang et al. 2006; Xia et al. 2010). Cav-1 is markedly downregulated in primary pulmonary fibroblasts and lung tissues from IPF patients, compared with controls (Wang et al. 2006). Furthermore, Cav-1 is able to inhibit the expression of TGF-β1 and PDGF (Yamamoto et al. 1999; Razani et al. 2001), and regulate TNF-α-induced endothelial cell activation and inflammation (Wang et al. 2008). This evidence concerns the gene CAV1 and idiopathic pulmonary fibrosis.