Our lab and others have shown that it is pro-angiogenic when acting through its receptor, Plexin-B1 on endothelial cells [3,4], and may be produced by malignancies in hypoxia or through aberrant expression of hypoxia inducible factor-1 for the purposes of promoting blood vessel growth into a tumor in a manner analogous to vascular endothelial growth factor [5]. The gene discussed is PLXNB1; the disease is neoplasm.