Since our current and previous data [18, 19]) suggest that it would be therapeutically desirable to maintain or activate EphB4 signaling in tumor cells while also inhibiting ephrinB2 reverse signaling in the vasculature, we examined the in vivo effects of a dimeric ephrinB2-Fc fusion protein in our MOC2 mouse model of metastasis. Here, EFNB2 is linked to neoplasm.