CXCR4 and acute myeloid leukemia: By using rapamycin to attenuate mTORC1 signaling during ex vivo expansion, the treated CAR T cells, compared to untreated CAR T cells, had elevated CXCR4 expression, enhanced bone marrow infiltration capacity, and augmented cytotoxicity against bone marrow resident leukemic cells in various xenograft models of human acute myeloid leukemia (AML).