The general overview presented here describes the role of AKT/mTOR in mediating mitochondrial metabolism through glucose in normal and deregulated pancreatic islet cells, how glycolysis and other energy producing mechanisms are used to support rapid tumor cell growth, and the emerging role of mTORC1 and mTORC2 in mediating signaling in response to metabolic stress that may result from these or other cellular contexts. This evidence concerns the gene MTOR and neoplasm.