KRAS and pancreatic neoplasm: The successful establishment of Cre/loxP-based pancreatic tumor models that express oncogenic KRAS predominantly in the exocrine pancreas was aided by two crucial technological advances: (1) the creation of the KrasLSL−G12D knockin line [113], which carries a transcriptional STOP sequence flanked by two loxP sites in front of the G12D mutant coding exon, and (2) the development of strains that express Cre recombinase under the control of promoters/enhancers of the Ptf1-p48 and Pdx1 genes [114, 115].