Chronic myeloid leukemia (CML) is a pluripotent stem cell disease, characterized by a reciprocal translocation between chromosomes 9 and 22, resulting in the fusion gene BCR–ABL. Since 1960, the year the Philadelphia chromosome was first described , there has been an enormous development in the understanding of the pathogenesis of CML. At the same time, treatments for CML have also changed dramatically. Nonspecific treatments, such as radiation, busulfan and hydroxyurea that were developed during the 20th century, were used successfully for controlling symptoms and blood counts, but did not change the natural course of the disease. IFN-α and hematopoietic stem cell transplantation (HSCT) were the first treatments to change cytogenetic status and improve survival. In 2001, the first tyrosine kinase inhibitor (TKI), imatinib mesylate, was approved for the treatment of CML. The introduction of TKIs has completely changed the way most patients with CML were treated and has immensely improved their prognosis. Following imatinib, other TKIs have been developed, including nilotinib, dasatinib, bosutinib and lately pomatinib, which is also effective against the T315I mutation. Despite the progress that has been made in the understanding of the pathogenesis of CML and the vast improvement in the management and treatment of CML patients, complete cure is still not feasible in most patients. HSCT is still considered the only curative treatment available.