Increased presence of HDAC9 has been reported to play a profibrotic role in the activation of hepatic stellate cells (HSC) during liver fibrosis in vivo, whereas knockdown of HDAC9 decreased TGF-β1-induced fibrogenic gene expression in the human HSC cell line LX-2 [50]. The gene discussed is TGFB1; the disease is Hepatic fibrosis.