The overall hypothesis guiding this work is mouse pancreatic ductal cells, which are otherwise refractory to transformation under conditions of physiologic oncogenic Krasmut expression, will become morphologically distinct PanIN or IPMN when expressing cKras. We predict if cKras is able to generate neoplastic and invasive PDAC that this model will provide important context and a new model to study molecular requirements for ductal derived PDAC. Here, KRAS is linked to pancreatic intraductal papillary-mucinous neoplasm.