Targeted mutation in the intestinal epithelium was induced through intraperitoneal administration of tamoxifen, with deletion of wild-type Kras in the context of oncogenic KrasG12D (AKrasfl/G12D) resulting in a significant acceleration of tumorigenesis, and a consequent reduction of median survival based upon an endpoint defined by clinical signs associated with tumour burden. Here, KRAS is linked to neoplasm.