HDAC9 and idiopathic pulmonary fibrosis: Further, similar to tumour cells, results from our group and other groups suggest that epigenetic histone modifications account for the aggressive phenotype and the persistent activated state of IPF fibroblasts [162,163,164,165], which indicated a “cancer-like” upregulation of almost all Class I and Class II histone deacetylase (HDAC) enzymes and (amongst other HDAC-induced activities) [165] the abnormal “malignant” repression of proapoptotic genes [163,164].