Given both NRP1 and NRP2 are known to modulate primary and secondary tumor microenvironments by interacting with integrins to remodel the tumoral ECM (20, 64, 66), of which FN is known as a major component (67), it follows that the impaired tumor growth exhibited following NRP codepletion likely arises as a result of perturbations in EDA-FN fibril assembly and deposition. The gene discussed is NRP2; the disease is neoplasm.