Specific HDAC gene silencing (HDAC1 through HDAC11, except HDAC6) by RNAi in TGF-β-stimulated IPF fibroblasts with the use of ACTA2 transcript levels as a readout parameter revealed that the silencing of HDAC7 by RNAi was the most effective in reducing TGF-β-induced ACTA2 expression in primary IPF fibroblasts [246]. Here, ACTA2 is linked to idiopathic pulmonary fibrosis.