Taken together, these data demonstrate a role for PRL-3 in mediating drug resistance in AML through Stat activation and upregulation of Mcl-1, and the down-regulation of PRL-3 accounts for much of the synergistic effect between SAHA and ABT-869, which is dependent on FLT3 signaling. This evidence concerns the gene SOAT1 and acute myeloid leukemia.