Alternatively, in a mouse model of acute promyelocytic leukemia, treatment with a CXCR4 antagonist made leukemia cells more sensitive to cytarabine and prolonged the survival of tumor-bearing mice compared to both untreated mice and mice treated with cytarabine alone [58], thus suggesting a role for CXCL12/CXCR4 inhibition in hematological malignancy treatment; therefore, there is the possibility that CXCR4 blockade could contribute to AML chemosensitization. The gene discussed is CXCL12; the disease is acute myeloid leukemia.