Interestingly, the activation of the PI3K/AKT/mTOR pathway is also related to other pathways in AML, namely FLT3-ITD mutations or mechanisms involving BCL2 and the cell survival and apoptosis pathway, which implies that the use of PI3K/AKT/mTOR inhibitors in monotherapy is severely limited. This evidence concerns the gene FLT3 and acute myeloid leukemia.