Primary IPF fibroblasts treated with the pan-HDAC inhibitor LBH589 and the Class I HDAC inhibitor valproic acid (VPA) can considerably reduce the profibrotic and antiapoptotic phenotypes owing to the regulatory effect of Class I HDACs, such as HDAC1, HDAC2, and/or HDAC3, on the expression of various key molecules that are antiapoptotic and profibrotic in lung fibroblasts (Korfei et al., 2015). The gene discussed is HDAC1; the disease is idiopathic pulmonary fibrosis.