Although these findings indicate that Wnt4 is an essential modulator of renal fibrosis development, the above-mentioned inconsistent results may suggest that the maintenance of Wnt4/β-catenin signaling in a balanced state may prevent the tubular EMT process and progression of renal interstitial fibrosis in DKD, but also signify that the effect of Wnt4 could additionally be mediated through the non-canonical Wnt signaling pathway, independent of β-catenin. Here, WNT4 is linked to diabetic kidney disease.