In our study, the post-treatment with a PPAR-β/δ agonist (GW0742) alone or combined with a PPAR-γ agonist (rosiglitazone) strongly decreased the amount of TGF-β1-mediated increase in intracellular COL1 (Fig. 3A–C) by affecting COL1A2 promotor activity (Fig. 3D) as well as extracellular collagen (Fig. 3E) in both, fibroblasts from control and IPF patients. The gene discussed is COL1A2; the disease is idiopathic pulmonary fibrosis.