Undoubtedly, there remains a need for further understanding of: (1) anticancer mechanisms of metformin, particularly those involving, but not limited to, mTOR signaling (upstream and downstream) and mitochondrial energy metabolism, (2) pharmacokinetic and pharmacodynamic properties of metformin, and (3) relationships between risk factors such as DM and development and progression of pancreatic cancer to identify further molecular targets and advance potential therapies. This evidence concerns the gene MTOR and familial pancreatic carcinoma.