In Diabetic Nephropathy (DN) [122], the increased expression of TGF-β1 has been shown to promote the accumulation of ECMs such as collagens and fibronectin, apoptosis, dedifferentiation of podocytes, and epithelial-mesenchymal transition of proximal tubules, all of which are considered to facilitate renal hypertrophy and dysfunction. This evidence concerns the gene FN1 and diabetic kidney disease.