First, ADC 513 caused increased phosphorylation of histone-H3Ser10 in AML blasts in vivo with minimal leucocytosis; second, the unconjugated antibody of ADC 711 (h17-NA) blocks CXCR4 but does not inhibit MOLP-8-derived tumour growth; third, the selective toxicity of ADCs 711 and 713 to specific CXCR4+ normal cells can be attributed, at least in part, to differences in cell proliferation rates (our data and42,43). This evidence concerns the gene CXCR4 and acute myeloid leukemia.