Smad2/3 complex, protein kinase C (PKC), p38 mitogen‐activated protein kinases (MAPK), interleukin like kinase (ILK) and Wnt/beta‐catenin signaling are among the downstream targets that mediate pro‐fibrogenic effects of TGFβ1 (Figure 6).[146, 147, 148, 149] Although evidence suggest that TGFβ1 has an established role in pathophysiology of diabetic kidney disease, therapies that target active TGFβ1 unfortunately fail to show efficacy in clinical studies. This evidence concerns the gene TGFB1 and diabetic kidney disease.