Bcr-Abl constitutively activates multiple signaling pathways such as Janus family of kinase/signal transducer and activator of transcription (JAK/STAT) pathway, and phosphatidylinositide 3-kinase/protein kinase B (PI3K/AKT) pathway [2–5], which results in cytokine independent proliferation, thereby leading to chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) [6, 7]. This evidence concerns the gene AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive.