STAT3 impairs the formation of Smad3–Smad4 complexes and reduces Smad3 binding to chromatin, resulting in inhibition of Smad3-mediated transcriptional activation, and cross-talk between JAK/STAT and TGF-β/Smad promotes the fibrosis of DKD (Lan, 2012; Wang et al., 2016). This evidence concerns the gene SMAD3 and diabetic kidney disease.