In addition, other workers have reported that i) CEACAM6 overexpression occurs in variety of epithelial malignancies[5-7], ii) that CEACAM6 overexpression is associated with increased metastases, proliferation and the suppression of annoikis[7-9], iii) that CEACAM6 overexpression induces a src-dependent increase in AKT activity that suppresses gemcitabine sensitivity in pancreatic cancer cells[9] and finally, iv) a transgenic model of CEA-overexpression suggests CEACAM6 overexpression can contribute to the development of colonic dysplasia[10]. This evidence concerns the gene AKT1 and pancreatic neoplasm.