bcr/abl kinase enables the CML cells to growth in a uncontrolled way by inducing p38 MAPK, Ras, Jun, PI-3K/Akt and STAT5 pathways, and blockage of bcr/abl kinase by imatinib mesylate has been recognized as the target therapy for CML [2,16–18]. The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.