CML patients commonly arise t(9;22)(q34;11) chromosomal translocation and formation of fusion gene BCR-ABL1, which is transcribed and translated into BCR-ABL1 protein with tyrosine kinase activity, thereby activating downstream signaling pathways such as PI3K-Akt-mTOR and MAPK, leading to abnormal cell proliferation [1, 3, 4]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.