Deletion of β-catenin in macrophages attenuated the ECM deposition and renal inflammation by limiting M2 macrophage polarization.375 Overexpression of Wnt9a drove tubular senescence and produce TGF-β1, which promoted proliferation and activation in normal rat kidney fibroblasts.376 Tubule-derived Wnts but not fibroblasts-derived Wnts were necessary for fibroblasts activation and renal fibrosis.377 Moreover, β-catenin expressed by TECs controlled the release of osteopontin (OPN) enriched exosome which promoted fibroblast proliferation and activation by binding to CD44.340. This evidence concerns the gene TGFB1 and renal fibrosis.