Inasmuch as src may be an important mediator of cross-talk between EGFR family members and several growth-modulating pathways such as Met, Notch-1 and furin [45]–[47], our findings suggest that concomitantly targeting the activation of cell-surface receptors such as EGFR, HER2, and TβRI and the intracellular src kinase may represent a novel strategy for suppressing pancreatic cancer growth in the presence of oncogenic Kras. This evidence concerns the gene FURIN and pancreatic neoplasm.