HDAC8 and pulmonary fibrosis: Taken together, these three studies involving animal models of lung fibrosis highlight the obviously potent antifibrotic efficacy of pharmacological inhibition or genetic knockdown of single Class I isoforms to block the evolvement of lung fibrosis (Table 2) and emphasise an underestimated dominant role of HDAC3 and HDAC8 in the pathogenesis of fibrotic lung disease.