The abnormally active BCR-ABL1 fusion protein was found to be the leading cause of Ph+CML, and specifically designed drugs targeting to inactive its function has been one of the most successful developments in molecular targeted therapy (Soverini et al., 2014). Imatinib mesylate was introduced in the 1990s as the first tyrosine kinase inhibitors (TKI) to treat Ph+CP-CML patients (Hehlmann et al., 2007). Imatinib binds to the inactive form of BCR-ABL1 and stops it from auto-phosphorylation, thus preventing the disease causing cascade of downstream effect (Pemovska et al., 2015). Currently, there are 5 TKIs approved by the US Food and Drug Administration (FDA) to be used in treating CML patients, including imatinib, dasatinib, nilotinib, bosutinib
