Inhibition of VEGF signaling reduces angiogenesis and slows tumor growth, but can also promote lymph node metastasis in some preclinical models. Studies of RIP-Tag2 transgenic mice revealed that inhibition of VEGF signaling by a function blocking anti-VEGF antibody or the receptor tyrosine kinase inhibitor sunitinib increased the number of intratumoral lymphatics, the proportion of lymphatics with tumor cells inside, and the incidence of lymph node metastasis. After the treatment, c-Met was upregulated in lymphatics in and around the tumors. Importantly, inhibition of c-Met by PF-04217903 administered with the angiogenesis inhibitor significantly reduced the abundance of intratumoral lymphatics, tumor cells inside lymphatics, and lymph node metastases. For details, see article by Sennino and colleagues on page 3692.