In a study investigating diabetic nephropathy, advanced glycation end-products (AGEs) are used to mimic diabetic conditions and AGEs lead to up-regulation of TGF-β1, CD40, and IL-17 in cultured human podocytes where co-stimulation of IL-17 and CD40L strongly activates TGF-β1 and CD40 expression [42]. The gene discussed is TGFB1; the disease is diabetic kidney disease.