The elevated activity of BCR-ABL tyrosine kinase initiates CML and approximately 30% of acute lymphoblastic leukemia (ALL) by stimulating proliferation signals, such as Ras, phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and signal transducer and activator of transcriptions (STATs) as well as by inhibiting apoptosis signals, such as Ras-dependent signaling pathway [3, 4]. The gene discussed is AKT1; the disease is acute lymphoblastic leukemia.