Given that clinical trials with FLT3 inhibitors have shown primary or secondary drug resistance (Wiernik, 2010) and the implication of PRL-3 in AML drug resistance (Zhou et al, 2011), we herein attempted to develop an alternative strategy by using PRL-3 antibody to target PRL-3 (an intracellular phosphatase) expressing AML cells. This evidence concerns the gene FLT3 and acute myeloid leukemia.