Altogether, the poor response to CXCR4 antagonism in AML is consistent with disappointing results from clinical studies and uncertainty about the group of patients that would benefit from this treatment strategy.13 While it has been proposed that stronger inhibitors than AMD3100 may improve treatment outcome,22, 23 our study suggests that the limited effectiveness of CXCR4 antagonists in AML might be partially explained by its mode of action being limited to blast mobilization, while lacking an effect on the behavior of parenchymal AML. The gene discussed is CXCR4; the disease is acute myeloid leukemia.