Although AML and ALL share alterations in signaling pathways that promote their proliferation, such as Wnt/β-catenin, PI3K/AKT/mTOR, NOTCH, and JAK/STAT [61,62], AML cells are characterized by high molecular heterogeneity that may favor the upregulation of other metabolic pathways such as NF-κB, Hedgehog, EGFR, TGF/SMAD, and PPAR contributing to their high replication rate [61,62]. This evidence concerns the gene AKT1 and acute myeloid leukemia.