AKT1 and acute myeloid leukemia: Moreover, inhibition of mTOR, both ex vivo and in vivo, did not induce upstream AKT-phosphorylation, indicating that a positive feedback mechanism, leading to activation of upstream PI3K/AKT signaling after mTOR inhibition described for malignancies with constitutive PI3K/AKT signaling including acute myeloid leukemia [27, 28], is not operative in TTLshort ALL.