In fact, two reports of exceptional responders to mammalian target of rapamycin (mTOR) inhibition were recently published, first, in a patient with Peutz–Jeghers syndrome and advanced pancreatic cancer,6 and second, in a single patient in a trial of an AKT inhibitor who was subsequently shown to have activating KRAS mutation and loss of PTEN.7 These studies suggest that there may be a therapeutic opportunity for inhibition of mTOR in selected patients with pancreatic cancer. This evidence concerns the gene AKT1 and pancreatic neoplasm.