Nuclear translocation of beta-catenin is seen in experimental models of nephrotic syndrome both in vitro and in vivo and also in diabetic nephropathy (41). Wnt signaling is responsible for the translocation of beta-catenin and plays an important role in podocyte injury and proteinuria (41). TGF-B1 treatment stimulates SNAIL expression in vitro. Additionally, ectopic expression of SNAIL induces changes in podocyte phenotype consistent with EMT (8). SLUG is also expressed following TGF-B1 treatment in vitro (7). Here, CTNNB1 is linked to nephrotic syndrome.