As expected, LBH589-treated IPF-fibroblasts indicated much more pronounced and excessive histone-acetylation compared to vehicle- and pirfenidone, due to efficient pan-HDAC inhibition, but was also associated with a depletion of HDAC1, -2, -6 and -9 on the post-translational level (which is often observed in response to [pan-]HDAC inhibition thereby potentiating repression of HDAC activity [64]), while transcript levels of HDAC1 and HDAC2 were slightly increased (presumably as compensatory mechanism). The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.