Further, the anti-apoptosis gene BIRC5/survivin, which is overexpressed in fibroblast foci of IPF-lungs and suspected to mediate apoptosis-resistance and persistence of myofibroblasts [65], was suppressed after LBH589-treatment, but also appeared to be partially downregulated in pirfenidone-treated IPF-fibroblasts. This evidence concerns the gene BIRC5 and idiopathic pulmonary fibrosis.