Moreover, A3B8 mAb-mediated AML cell proliferation inhibition, as well as in some cases the induction of differentiation, is accompanied by a marked decrease in the phosphorylation of the mammalian target of rapamycin complexes (mTORC)1 and 2, which is strongly correlated with the inhibition of the PI3K/Akt pathway [29]. This evidence concerns the gene AKT1 and acute myeloid leukemia.