BCR-ABL1 fusion gene, produced by the specific t (9;22) (q34;q11) chromosomal translocation, occurs in approximately 90% of the chronic myeloid leukemia (CML), 25% of the acute lymphoblastic leukemia (ALL) and less than 5% of the acute myeloid leukemia (AML) cases [1–3], and it constitutively encodes tyrosine kinase BCR-ABL1 oncoprotein, which is responsible for proliferative signals and leukemogenesis by activating Raf/MEK/ERK, PI3K/AKT, and JAK/STAT pathways [4, 5]. This evidence concerns the gene AKT1 and acute myeloid leukemia.