CXCR4 and neoplasm: Utilizing this insight to harness the selectively upregulated E-selectin on endothelial cells in the AML BM niche, together with overexpression of gain-of-function (GoF) CXCR4, CXCR4R334X, we show that the significant reduction of NK cell BM infiltration in animals with high AML burden is almost restored to that of non-tumor-bearing animals.