Several pathways are initialized and further sustained by BCR-ABL1 kinase, including Janus kinase (JAK)/signal transducer and activator of transcription (STATs), phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPK), extracellular-signal-regulated kinase (ERK), etc. However, the introduction of TK inhibitors (TKI) has led to a major advancement in CML treatment [6,7]. This evidence concerns the gene TKT and chronic myelogenous leukemia, BCR-ABL1 positive.