Targeting profibrotic myofibroblasts as a therapeutic approach to the treatment of pulmonary fibrosis has been suggested and tested [52]; however, our data for the first time demonstrates antifibrotic effects of SDF-1β overexpression, not only by affecting myofibroblasts but also by inducing alveolar epithelial cell proliferation, therefore making it a very promising candidate for lung remodeling and treatment of IPF. This evidence concerns the gene CXCL12 and pulmonary fibrosis.