The expression of TGF-β1 is increased in endothelial cells, which, in turn, triggers the activation of TGF receptors, namely TGFBR2 and TGFBR3, on B lymphocytes, podocytes, glomerular endothelial cells, and mesangial cells, leading to epithelial–mesenchymal transition and fibrosis in the development of diabetic nephropathy [17,57,59]. Here, TGFBR2 is linked to diabetic kidney disease.