Manipulation of these pathways has been reported to endow CD8+ T cells with greater antitumor ability, consistent with the roles of mTORC1/mTORC2 in dictating CD8+ T-cell fate; rapamycin pretreatment of CAR-T cells during ex vivo expansion reduced mTORC1 activity while increasing CXCR4 expression, allowing these cells to infiltrate bone marrow and reduce resident AML cells [80]. The gene discussed is CD8A; the disease is acute myeloid leukemia.