We have recently reported that lung fibroblasts from patients with IPF exhibit a profibrotic phenotype with “cancer-like features” due to the abnormal overexpression of all Class I and Class II HDAC enzymes, which appeared responsible for their aberrant activation and persistence in IPF, presumably as the result of changes in expression profiles and cellular signalling due to alterations in the acetylation status of the chromatin and various non-histone proteins [165]. The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.