Zhang and co-workers report on the renoprotective role of the vitamin D receptor (VDR) in diabetic nephropathy using the method of streptozotocin-induced hyperglycemia in wild-type and VDR(-/-) mice. Also, experiments with cultured mesangial cells and podocytes confirm the effect of the active vitamin D metabolite 1,25(OH)(2)D(3) on inhibition of the renin-angiotensin system (RAS) in vitro. The authors conclude that the higher activation of the intrarenal RAS is the key factor to induce more severe diabetic nephropathy in VDR(-/-) mice.