While the NRP1-ΔE4 is dominantly expressed in CRC associated with tumor progression, both NRP1 splice variants are defective in N-linked glycosylation modification, and exhibit increased endocytosis/recycling activity with decreased levels of degradation, which lead to their accumulation on endosomes and persistent activation of FAK/p130Cas signaling through interaction and co-internalization with Met and β1-integrin. This evidence concerns the gene PTK2 and neoplasm.