By recruiting the adaptor proteins such as Grb24, 5 and CrkL6, 7, BCR-ABL activates several signaling pathways, including PI3K-Akt, MAPK4, 8, 9, 10 and STAT511, thus leading to uncontrolled cell proliferation and CML pathogenesis8, 12. This evidence concerns the gene AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive.