Moreover, the abovementioned preclinical studies in lung fibrosis reveal that HDAC inhibitors may also offer a new therapeutic strategy in IPF by blocking fibrotic remodelling through (i) suppression of profibrotic gene expression, (ii) restoration of antifibrotic genes and (iii) increasing myofibroblast susceptibility to apoptosis. Here, HDAC9 is linked to pulmonary fibrosis.