A genetic study mapped broad, convergent resistance mechanisms to asciminib in chronic myeloid leukemia (BCR::ABL1), identifying 279 resistance mutations. The work showed that escape can come from alterations spread across much of the BCR::ABL1 protein, including changes in regulatory regions outside the drug-binding pocket. By building a resistance landscape for asciminib, the analysis gives clinicians and developers a clearer playbook for anticipating failure modes and for designing next-generation inhibitors or combination approaches that target multiple resistance pathways.