Nevertheless, HDAC4-mediated regulation of profibrotic signaling may not be limited to the TGF-β1/Smad3 pathway since we found that pharmacological and genetic inhibition of HDAC4 also reduced phosphorylation of STAT3 and ERK1/2, two pathways that also regulate multiple profibrotic processes (i.e., renal fibroblast activation, EMT, and inflammation) and lead to renal fibrosis. This evidence concerns the gene SMAD3 and renal fibrosis.