KRAS and pancreatic adenocarcinoma: Likewise, pancreatic adenocarcinoma has been generated by sequential mutagenesis, where first KrasFRT-STOP-FRT-G12D and Rosa26FRT-STOP-FRT-Cre-ER-T2 are recombined by Pdx1-Flp to generate pancreatic tumors harboring oncogenic KRAS and the Cre-ERT2 fusion protein, then tamoxifen is delivered to the animal to activate Cre-ERT2 to recombine p53FL/FL in the pancreatic tumors, resulting in pancreatic tumors with both KRAS and p53 mutations (Schönhuber et al., 2014).