Thus, strategies aimed at blocking endocytosis or formation of NRP1 variants/Met/β1-integrin complexes or alternatively inhibiting their endosomal signals on activation of FAK/p130Cas pathway using pharmacological inhibitors of FAK, may have therapeutic potential in CRC and possibly other types of cancers with expression of the N-glycosylation-defective NRP1 splice variants. This evidence concerns the gene PTK2 and cancer.