In agreement, treatment of IPF fibroblasts with the well-characterised pan-HDAC inhibitor panobinostat resulted in the restoration of COX2 and CXCL10 expression through the creation of an active chromatin structure at their promoters, manifested as the accumulation of acetylated histones H3 and H4 [162,247]. This evidence concerns the gene HDAC9 and idiopathic pulmonary fibrosis.