HDAC6 and idiopathic pulmonary fibrosis: Moreover, in our study, pirfenidone prevented production of collagen-I and other profibrotic molecules in the presence of increased HDAC6 and concomitant significant reduction of α-tubulin acetylation in treated IPF-fibroblasts, thus clearly indicating that targeting α-tubulin deacetylation does not affect myofibroblast differentiation.