In 2015, Korfei et al. reported that lung fibroblasts derived from patients with IPF exhibited significantly elevated expression of Class I HDAC enzymes, leading to their aberrant activation and persistence in IPF due to alterations in the chromatin acetylation status and the acetylation of various non-histone proteins [18]. The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.