We previously found that there is a subgroup of up to 20% of human PDAC in which increased activation of AKT/mTOR is associated with poor survival.14 And in sleeping beauty screens using the Kras-driven pancreatic cancer model, Pten ‘hits’ were the most common, reinforcing how important deregulation of mTOR might be in driving PDAC.13, 14 Here, using a preclinical mouse model of PTEN-deficient PDAC, we have shown that survival can be significantly extended using the classical inhibitor of mTORC1, rapamycin, and this is associated with a proliferative arrest. This evidence concerns the gene MTOR and pancreatic neoplasm.