We recently demonstrated that ectopic Myc expressed at quasi-physiological levels is sufficient to drive immediate and synchronous transition of stalled, indolent KRasG12D-driven lung AAHs or pancreatic PanINs into, respectively, aggressive and invasive lung and pancreatic adenocarcinomas, along with all the signature stromal sequelae associated with each adenocarcinoma type37,38. This evidence concerns the gene MYC and pancreatic adenocarcinoma.