Regarding the strong HDAC inhibitor LBH589, which induced α-tubulin hyperacetylation in treated IPF-fibroblasts, we suggest that inhibition of profibrotic signaling was mainly due to strong histone acetylation and chromatin-transcription, as well as interference with signal transduction mechanisms (such as STAT3 pathway) mediated by HDACs. This evidence concerns the gene HDAC9 and idiopathic pulmonary fibrosis.