STAT3 protein was chosen because of its role as one of the downstream effectors of signaling pathways activated by BCR-ABL1 kinase leading to the transformation of CML, as well as results of the studies indicating that downregulation of STAT3 phosphorylation correlates with the induction of apoptosis of CML cells especially those that are resistant to TKIs. Here, BCR is linked to chronic myelogenous leukemia, BCR-ABL1 positive.