Before exploring this approach in tumor-bearing animals, we first characterized how the CXCR4/SDF-1α axis affects homing of human NK cells to BM compartments of nontumor-bearing NOD.Cg-PrkdcscidIl2rgtm1WjlTg(CMV-IL3,CSF2,KITLG)1Eav/MloySzJ (NSG-SGM3) mice, as this strain is slightly different from the NSG used in previous work.7 Healthy donor blood NK cells were expanded as previously described8 followed by either mRNA transfection to transiently express CXCR4R334X at high levels or CRISPR/Cas9-mediated CXCR4 gene knock-out (KO) to diminish expression (Figure 1A; Suppl. The gene discussed is CXCR4; the disease is neoplasm.