In this respect, even if, as conceivable, VEGF-A and SEMA3A promote NRP1 internalization19, we have previously shown that, in ECs, NRP1 displays the ligand-independent ability to associate with and promoting the endocytosis of active α5β1 integrin20, the main fibronectin (FN) receptor driving embryonic vascular development and cancer angiogenesis21, thanks to the interaction of its short cytosolic tail with trafficking adaptors, such as GIPC1. The gene discussed is NRP1; the disease is cancer.