However, our findings were contrary to those of a previous in vitro study, which showed that TGF-β1 treatment enhances Akt2 expression in HK-2 cells and that deletion of the Akt2 gene suppresses TGF-β1-induced epithelial-mesenchymal transition (EMT) 28, which is thought to contribute to renal fibrosis in DN. Here, TGFB1 is linked to renal fibrosis.