HDAC9 and idiopathic pulmonary fibrosis: Results from our group and others suggest that specifically epigenetic mechanisms and histone modifications account for the aggressive phenotype of fibrotic fibroblasts, which indicated ‘cancer-like’ upregulation of various HDAC enzymes, and that HDAC inhibitors may offer a new therapeutic strategy in IPF by increasing myofibroblast susceptibility to apoptosis and blocking fibrotic remodelling [31–33,60].