In one key study, Zeisberg and colleagues [4] showed in three mouse models including unilateral ureteral obstructive nephropathy (UUO), Alport disease and streptozotocin-induced diabetic nephropathy, that around 30% to 50% of fibroblasts formed in the kidneys co-expressed the endothelial marker CD31 and the fibroblast/myofibroblast markers fibroblast specific protein-1 (FSP-1) and/or α-smooth muscle actin (α-SMA). This evidence concerns the gene S100A4 and diabetic kidney disease.