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]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.