Recently, published work highlights a crucial role of single Class I HDAC enzymes, in particular HDAC3, in progressive fibrotic lung diseases as the HDAC3-selective inhibitor RGFP966 effectively reduced pulmonary fibrosis in bleomycin-treated wild-type mice and conditional Hdac3(−/−) mice were largely resistant to bleomycin-induced lung fibrosis [258]. The gene discussed is HDAC3; the disease is lung disorder.