In several genetically engineered mouse models, oncogenic KRAS expression in pancreatic epithelial cells has been shown to be necessary for disease initiation and maintenance through cell-autonomous actions (e.g., regulation of cell proliferation, differentiation, metabolism, and replicative senescence) and non-cell autonomous remodeling of both premalignant and tumor microenvironment (TME) (reviewed in [8]). This evidence concerns the gene KRAS and neoplasm.