In CML, HCK is activated by BCR/ABL, an oncogenic fusion protein in a large majority of CML as well as in some acute lymphocytic leukemia, leading to the persistent activation of STAT5 and its excessive accumulation in the cytoplasm, where STAT5 activates AKT through combining with PI3K and the adaptor protein GAB2, promoting cell growth and survival [14,15]. This evidence concerns the gene GAB2 and chronic myelogenous leukemia, BCR-ABL1 positive.