To establish the therapeutic potential of PPAR-γ ligands we treated fibroblasts obtained from IPF patients, in parallel, with PPAR-γ ligands, two PI3K inhibitors and a FAK inhibitor and confirmed that CDDO and 15d-PGJ2 potently block myofibroblast differentiation of not only normal HLF but also diseased IPF fibroblasts (Fig 7) via PI3K-Akt and FAK pathways. This evidence concerns the gene PTK2 and idiopathic pulmonary fibrosis.