It was also found that 17-N-allylamino-17-demethoxygeldanamycin (17-AAG), a small-molecule inhibitor of Hsp90, inhibited TGF-β1-induced myofibroblast transformation and ECM production in primary lung fibroblasts in vitro and abolished significantly myofibroblast accumulation, ECM deposition and fibrotic tissue generation in the bleomycin- as well as TGFα mouse model of pulmonary fibrosis in vivo [13,16]. Here, TGFB1 is linked to pulmonary fibrosis.