Small-molecule inhibitors, short peptides, and antibodies have been developed to disrupt the CXCL12/CXCR4 axis that releases AML blasts from the BM [63], and recent findings suggest that CXCR4 antagonism can potentially synergize with immunotherapies in several clinical trials involving solid tumors. The gene discussed is CXCL12; the disease is acute myeloid leukemia.