Moreover, in vitro studies in rat tubular epithelial cells (NRK52-E cell line) showed that HDAC inhibition by the HDAC inhibitor Trichostatin A (TSA), valproic acid, SK-7041, or N-acetylcysteine or gene silencing of HDAC-1/2 restored TGF-β1-induced phenotypic changes, including induction of α-SMA and loss of epithelial markers [64], suggesting that histone acetylation could also be involved in renal fibrosis by modulating the epithelial phenotype. This evidence concerns the gene HDAC9 and renal fibrosis.