The FLT3 gene is frequently mutated and thereby encodes a constitutively activated kinase in human AML and is an adverse prognostic factor [93]; this FLT3-initiated signaling is mediated through different pathways (including PI3K-Akt-mTOR) and CDC25 may thereby mediate or contribute to the adverse prognostic impact of this genetic abnormality. This evidence concerns the gene MTOR and acute myeloid leukemia.