In conclusion, endogenous VASH2 may exacerbate urine albumin excretion and mesangial expansion in diabetic nephropathy, possibly through enhancing VEGFR-2 signaling in glomerular endothelial cells and ECM production in mesangial cells, thus indicating that VASH2 could represent a potential therapeutic target for diabetic nephropathy. This evidence concerns the gene ALB and diabetic kidney disease.