In the context of ductal adenocarcinoma of the pancreas, recent mouse models have shown that pancreatic ductal cells can serve as the cell of origin of PDAC when Kras is mutated and, from the onset of oncogenic Krasmut expression, Trp53, Fbw7, or Pten are genetically deleted, or a gain of function mutant of Trp53 is expressed, using Hnf1b:CreERT2, Sox9:CreER, or Ck19:CreER driver lines [4, 17, 22, 41, 42]. This evidence concerns the gene KRAS and pancreatic ductal adenocarcinoma.