Much to our surprise, pirfenidone only was capable in reducing transcription of profibrotic ECM-associated genes CNN1 (calponin), DES (desmin) and P4HTM (transmembrane prolyl 4-hydroxylase) as compared to LBH589- and vehicle-treatment, with CNN1 and DES being paradoxically even upregulated in IPF-fibroblasts in response to LBH589. This evidence concerns the gene DES and idiopathic pulmonary fibrosis.