Since SDF1 has been shown to mediate migration of AML in a CXCR4 dependent mechanism and that SDF1/CXCR4-induced migration is dependent on activation of downstream BTK in CLL, myeloma and normal B cells [21, 27], we examined the activity of BTK phosphorylation and downstream AKT and MAPK in response to SDF1 and found that SDF1 increases levels of pBTK and downstream MAPK in primary AML blasts (Figure 2A). This evidence concerns the gene AKT1 and acute myeloid leukemia.