Since our current and previous data (Bhatia et al., 2022; Bhatia et al., 2019) 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. The gene discussed is EPHB4; the disease is neoplasm.