This study investigates the role of mTOR, the mammalian target of rapamycin, in regulating memory CD8 T cell differentiation. Surprisingly, rapamycin, an mTOR inhibitor, was found to enhance the generation of virus-specific CD8 T cells in mice infected with lymphocytic choriomeningitis virus (LCMV) and in mice vaccinated with a non-replicating VLP-based vaccine. Rapamycin treatment also improved the functional qualities of memory CD8 T cells, as evidenced by increased homeostatic proliferation and better recall responses. The effects of rapamycin were observed during both the expansion and contraction phases of the T cell response, suggesting that it enhances the formation of memory precursors and accelerates the memory differentiation program. Further experiments using RNAi to inhibit mTOR, raptor, or FKBP12 in antigen-specific CD8 T cells confirmed that mTOR acts intrinsically through the mTORC1 pathway to regulate memory T cell differentiation. These findings identify a molecular pathway that regulates memory formation and provide a strategy for improving the functional qualities of vaccine-induced or infection-induced memory T cells.This study investigates the role of mTOR, the mammalian target of rapamycin, in regulating memory CD8 T cell differentiation. Surprisingly, rapamycin, an mTOR inhibitor, was found to enhance the generation of virus-specific CD8 T cells in mice infected with lymphocytic choriomeningitis virus (LCMV) and in mice vaccinated with a non-replicating VLP-based vaccine. Rapamycin treatment also improved the functional qualities of memory CD8 T cells, as evidenced by increased homeostatic proliferation and better recall responses. The effects of rapamycin were observed during both the expansion and contraction phases of the T cell response, suggesting that it enhances the formation of memory precursors and accelerates the memory differentiation program. Further experiments using RNAi to inhibit mTOR, raptor, or FKBP12 in antigen-specific CD8 T cells confirmed that mTOR acts intrinsically through the mTORC1 pathway to regulate memory T cell differentiation. These findings identify a molecular pathway that regulates memory formation and provide a strategy for improving the functional qualities of vaccine-induced or infection-induced memory T cells.