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)2D3 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.