Smad 3 acetylation has been implicated in the pathogenesis of DN recently [49, 50], overexpression of transcription factor SREBP-1 induces glomerulosclerosis of DN; SREBP-1a K333 acetylation by CBP is required for Smad3 association and SREBP-1 transcriptional activity; both Smad3 and SREBP-1a activation regulates TGF-β1 transcriptional responses associated with DN, SREBP-1 inhibition could be a novel therapeutic strategy for DN [49]. This evidence concerns the gene SREBF1 and liver dysplastic nodule.