Because Hoxa9 and Meis1 overexpression is frequent in high-risk AML (Drabkin et al., 2002, Heuser et al., 2009, Zangenberg et al., 2009), and because both factors are currently considered undruggable, we set out to elucidate the effects of combined Hoxa9/Meis1 overexpression on intracellular signaling and to investigate whether cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling processes. This evidence concerns the gene MEIS1 and acute myeloid leukemia.