Chronic myeloid leukemia (CML) is a clonal stem cell neoplasm characterized by the presence of the Philadelphia (Ph) chromosome.1 The Ph chromosome produces the breakpoint cluster region‐Abelson murine leukemia (BCR‐ABL) fusion protein, which dysregulates tyrosine kinase activity and induces uncontrolled proliferation of the granulocyte lineage. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.