We have recently shown that while neurotensin, a GPCR agonist, activates ERK and Akt in an EGFR-independent way in pancreatic cancer Panc-1 cells, as also found by others [63], and activates ERK and Akt via EGFR transactivation in the colon cancer cell line HT 29, neurotensin uses both EGFR-dependent and -independent pathways in the colon cancer cell line HCT 116 [12]. This evidence concerns the gene EGFR and pancreatic neoplasm.