Interestingly, AML cells that escape from Akt-induced FOXO inactivation or loss of FOXO expression, become sensitive to JNK inhibitors, suggesting that JNK activation probably favors the selection of AML cells capable to withstand the loss of FOXOs, providing a rationale for the employment of JNK inhibitors in antileukemic therapy. This evidence concerns the gene AKT1 and acute myeloid leukemia.