Here we show for the first time that in human AML ibrutinib inhibits SDF1/CXCR4 pathway and functions to disrupt migration signals from the microenvironment This study further validates an emerging focus of targeting kinases critical for the survival of malignant cells and gives us a clearer understanding of how inhibition of BTK may optimally be harnessed therapeutically in AML. This evidence concerns the gene BTK and acute myeloid leukemia.