Since COX-2 silencing in F-IPF is critically associated with histone deacetylation and methylation [3,5], we then investigated whether changes in H3 acetylation and H3K27me3 state at the COX-2 promoter contributed to COX-2 downregulation in TGF-β1-activated fibroblasts and whether the effect of SAHA was mediated by epigenetic regulation. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.