Based on the genetic mutation profile and the deregulation of certain signaling pathways, such as FLT3 internal tandem duplication (FLT3-ITD), c-KIT, PI3K/AKT pathway, and non-coding RNAs, different targeted therapies have been developed to induce tumor-specific killing effect in AML [5–7]. This evidence concerns the gene AKT1 and acute myeloid leukemia.