Previous studies have demonstrated that biliary IGF-1 was 15–20 fold higher in patients with extrahepatic cholangiocarcinoma compared to levels in patients with pancreatic carcinoma or benign disease with an AUC of 1.[32] CEACAM6 overpression in pancreatic cancer is known to increase IGF-1 mediated cellular invasiveness through an Akt and Src-dependent pathway. Here, SRC is linked to pancreatic neoplasm.