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. The gene discussed is PTP4A3; the disease is acute myeloid leukemia.