Given that increased acetylation by HDAC inhibition reduces collagen production in different fibroblast types, new anti-fibrotic drug (suberoylanilide hydroxamic acid) acting as a histone deacetylase inhibitor (HDACi) appeared to be a promising therapeutic option in IPF by reducing collagen deposition [22, 23]. The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.