For example, administration of soluble monomeric EphB4 extracellular domain, which interferes with the binding of ephrin-B2 to EphB receptors and inhibits bidirectional signaling, was shown to inhibit tumor growth and tumor angiogenesis in several mouse tumor xenograft models as well as neovascularization in a model of retinopathy [28], [29], [30], [31], [32]. This evidence concerns the gene EPHB4 and neoplasm.