The BCR-ABL fusion protein is an abnormal protein produced by a genetic mutation that occurs during the formation of certain blood cells. This mutation results from a translocation between chromosomes 9 and 22, leading to the fusion of the BCR gene on chromosome 22 and the ABL gene on chromosome 9. The presence of this protein is a hallmark of chronic myeloid leukemia (CML) and some other types of leukemia. The BCR-ABL fusion protein has increased tyrosine kinase activity, which promotes uncontrolled cell division and inhibits normal apoptosis, or programmed cell death. This abnormal signaling contributes to the development and progression of leukemia. Targeted therapies, such as imatinib, have been developed to inhibit the activity of the BCR-ABL protein, providing effective treatment options for patients with CML.