Pathways involving epithelial cells and fibroblasts have been considered to be dominant in the pathogenesis of idiopathic pulmonary fibrosis (IPF), rather than an inflammatory response, even though the latter is actually the common process of most interstitial lung diseases (1). Although there are various initiating factors or causes for IPF, the terminal stages are characterized by fibroblast proliferation and the accumulation of connective tissue replacing normal, functioning parenchyma. In this context, myofibroblasts play a crucial role in the progression of fibrosis. Myofibroblasts arise from the differentiation of fibroblasts under the effect of transforming growth factor ß (TGF-ß), plateletderived growth factor, and other fibrogenic cytokines. They produce fibrogenic molecules, such as tissue inhibitor of metalloproteases and fibrogenic growth factor, as well as proapoptotic molecules that affect the epithelium, such as angiotensin II.