CD8A and acute myeloid leukemia: Consistent with the roles of mTORC1/mTORC2 in dictating CD8+ T-cell fate, manipulating these pathways has been reported to endow CD8+ T cells with greater antitumor ability: pretreatment of CAR-T cells with rapamycin during the ex vivo expansion stage reduced mTORC1 activity and upregulated the expression of CXCR4, allowing these cells to infiltrate bone marrow and eliminate resident AML cells [233].