Following 24 h TGF-β1 stimulation, treatment with PPAR-β/δ agonist alone or in combination with the two other members of the PPAR protein family inhibited the TGF-β1-mediated increase in COL1 and—to a lesser extent—α-SMA protein levels in control and IPF fibroblasts (Fig. 3A). This evidence concerns the gene ACTA1 and idiopathic pulmonary fibrosis.