Aside from ACTA2, the knockdown of HDAC7 by RNAi resulted in a significant reduction of TGF-β-upregulated profibrotic mediators NOX4 and CTGF in stimulated IPF fibroblasts, while expression of the TGF-β-suppressed antifibrotic gene PGC1A was increased. The gene discussed is ACTA2; the disease is idiopathic pulmonary fibrosis.