In CML, with the stimulation of BCR-ABL kinase activity, ERK1/2 is over-activated in the cytoplasm and exerts the oncogenic potential by enhancing the activities of anti-apoptosis proteins, such as Bcl-2, p-BAD, Bcl-XL, and Mcl-1, and inhibiting pro-apoptotic proteins, such as Bad and Bim (39, 51). Here, MCL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.