Since SMAD3is a key player in TGFβ1 signaling, its deactivation impairsHDAC6-dependent deacetylation of α-tubulin, highlighting thecrucial importance of HDAC6 in EMT through the TGF-β1–SMAD3signaling pathway.19 Several lines of evidencedemonstrated the effectiveness of pan-HDAC inhibitors (including romidepsin,SAHA, and panobinostat) against idiopathic lung fibrosis (IPF) andfibrotic diseases, mainly based on the decrease of myofibroblast differentiationand fibroblast proliferation prompted by TGF-β1.166−168 More recent reports pointed out the efficacy of a targeted HDAC6approach in IPF. This evidence concerns the gene HDAC6 and idiopathic pulmonary fibrosis.