Although we did not perform a dose-response transduction experiment with lentivirus, our results consistently supported that i) miR-29a modulates both DKK1/Wnt/β-catenin signaling and TGF-β1-mediated fibrosis in renal tissues, and ii) restoration of miR-29a and its downstream signaling is beneficial for improving diabetes-mediated renal fibrosis. Here, TGFB1 is linked to diabetes mellitus.