As such, the data summarized in this review suggest that EVs might participate in DKD development and progression by regulating molecular pathways related to fibrosis, either by carrying fibrosis-related molecules or by inducing the expression or the activation of different fibrosis associated pathways (e.g., TGF-β/smad3, Wnt/β-catenin or mTOR) in target cells. This evidence concerns the gene SMAD3 and diabetic kidney disease.