Bcr-Abl is an abnormal fusion protein resulting from the chromosomal translocation t(9;22)(q34;q11), which leads to the fusion of the BCR and ABL genes. This fusion protein exhibits aberrant tyrosine kinase activity and is predominantly localized in leukemia cells, especially in chronic myeloid leukemia (CML) and certain cases of acute lymphoblastic leukemia (ALL). Bcr-Abl activates multiple signaling pathways, including MAPK, PI3K/Akt, and JAK/STAT, promoting cell proliferation, inhibiting apoptosis, and resulting in the excessive growth and accumulation of leukemia cells. Specific expression of the Bcr-Abl fusion gene and certain mutation forms, such as T315I, confer resistance to certain tyrosine kinase inhibitors, posing a significant challenge in the treatment of CML.