Due to the dysregulation of the molecular pathways involved in the pathogenesis of AML, the use of mitogen-activated protein extracellular kinase 1/2 (MEK 1/2) and mammalian target of rapamycin (mTOR) inhibitors in AML therapy has been evaluated, but clinical trials have not achieved satisfactory clinical effectiveness with the aforementioned agents [8,9]. This evidence concerns the gene MAP2K1 and acute myeloid leukemia.