ABL1 is a non-receptor tyrosine kinase that orchestrates diverse cellular processes including cytoskeleton remodeling, cell adhesion and motility, receptor endocytosis, autophagy, DNA damage response, and apoptosis 12. ABL1 phosphorylates key cytoskeletal regulators like WASF3 to stimulate lamellipodia formation and migration, and coordinates actin dynamics through multiple substrates 1. The kinase regulates receptor tyrosine kinase trafficking and stability, including EGFR endocytosis and PDGFRB-mediated chemotaxis modulation. In the nucleus, ABL1 participates in DNA damage response by phosphorylating repair proteins and proapoptotic factors including TP73 and CASP9 [UniProt]. ABL1 also targets mitochondria during oxidative stress to mediate cell death 2. Clinically, ABL1 dysregulation drives hematologic malignancies. The BCR::ABL1 fusion generated by the Philadelphia chromosome 9(9;22) translocation causes chr9 myeloid leukemia (CML), characterized by explosive clonal expansion beginning 3-14 years before diagnosis 34. BCR::ABL1-positive acute lymphoblastic leukemia (ALL) and Philadelphia chr9-like ALL represent high-risk leukemias with activated kinase signaling 5. Multiple tyrosine kinase inhibitors (imatinib, nilotinib, dasatinib, bosutinib, asciminib, ponatinib) target BCR::ABL1, though acquired mutations in the kinase domain confer resistance to ATP-competitive inhibitors 467. Beyond leukemias, ABL1 alterations associate with dermatofibrosarcoma protuberans and follicular lymphoma, while dysregulated ABL1 expression appears relevant to endometriosis pathogenesis 8.