Huselton et al. [90] revealed that combining the CXCL12/CXCR4 inhibitor DSTAT with azacytidine benefits MDS and refractory acute myeloid leukemia (AML) patients, indicating that CXCL12 and CXCR4, as the upregulated cell adhesion molecules for leukemia stem cells, enables the immune escape of blood tumor cells within the bone marrow microenvironment. The gene discussed is CXCL12; the disease is myelodysplastic syndrome.