In a recent study, we used mouse tumor models expressing NRP1 or not, to establish the concept of a distinct, productive signaling pattern induced when VEGFR2 and NRP1 are co‐expressed on endothelial cells (denoted cis) compared with arrested signaling when the two molecules are expressed on adjacent endothelial (VEGFR2) and tumor (NRP1) cells (denoted trans). The gene discussed is KDR; the disease is neoplasm.