HDAC inhibitors have also been demonstrated to reverse repressive histone hypermethylation as ChIP assays revealed that SAHA treatment of IPF fibroblasts resulted in an enrichment of the pro-apoptotic BAK gene with acetylated lysine 9 on histone H3 (H3K9Ac), an active chromatin mark, and the depletion of BAK with H3K9Me3, thereby corresponding to increased BAK expression in the “corrected” IPF fibroblasts [164]. The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.