The tumstatin (T8) peptide significantly suppressed the STZ-induced increase in VEGF-A and VEGFR-2 in the renal cortex, suggesting that the therapeutic effect of the tumstatin (T8) peptide in early diabetic nephropathy may be at least partly attributable to the inhibition of excessive activation of VEGF-A signaling, analogous to previous studies using neutralizing anti-VEGF-A antibodies [19,20]. The gene discussed is KDR; the disease is diabetic kidney disease.