Our previous data indicated that the anti-VEGFR-1 D16F7 mAb generated in our laboratories is able to inhibit melanoma and glioblastoma cell chemotaxis in response to PlGF and VEGF-A and that this activity translates to efficient antitumor activity in preclinical in vivo models, even when mAb is administered as a single agent [17,18,19,20]. The gene discussed is FLT1; the disease is melanoma.