AKT1 and acute myeloid leukemia: Taken together, these data suggest a potential role of PI3K/AKT signaling in the mechanism of resistance to GO or, by extension, calicheamicin-γ1-induced cytotoxicity, thus raising the possibility of using inhibitors of this signaling pathway as a novel means to increase the sensitivity of AML cells to calicheamicin-γ1-based therapies.