FLT3 and acute myeloid leukemia: PRL-3, a phosphatase that we identified in 1998 (Zeng et al, 1998), was recently found as part of a core gene signature that is uniquely down-regulated by combination therapy of Linifanib (ABT-869, a FLT3 inhibitor) and suberoylanilide hydroxanic acid (SAHA, a histone deacetylase inhibitor) in AML cells (Zhou et al, 2011).