The advent of targeted therapies, particularly tyrosine kinase inhibitors (TKIs), has revolutionized the treatment of CML. Drugs such as imatinib (Gleevec) specifically inhibit the BCR-ABL tyrosine kinase, effectively halting the abnormal signaling pathways and proliferation induced by the fusion protein. These TKIs have dramatically improved the prognosis and quality of life for patients with CML, turning what was once a fatal disease into a manageable chronic condition.
