Activation of AKT or deletion of the FOXOs caused myeloid maturation and apoptosis in AML cells, but this effect was countered by a resistance mechanism in which c-JUN was activated, so a combination of FOXO and JNK (c-JUN N-terminal kinase) inhibition may be an effective therapeutic strategy (Sykes et al., 2011). This evidence concerns the gene AKT1 and acute myeloid leukemia.