One limiting factor in the development of targeted therapies for patients with pancreatic cancers is that most cancers are initiated secondary to a mutation in the KRAS gene.8, 9, 10, 11, 12 Murine models have been vital to establishing the role of mutant KRAS in pancreatic metaplasia, premalignant lesions and invasive ductal adenocarcinoma.13, 14, 15, 16 Unfortunately, to date an effective means to target mutant KRAS has yet to be established. This evidence concerns the gene KRAS and pancreatic neoplasm.