The acquisition of the oncoprotein Breakpoint Cluster Region-Abelson (BCR::ABL1), a constitutively active tyrosine kinase, induces leukemogenesis of chronic myeloid leukemia (CML), which progresses from the chronic phase (CP) to the accelerated phase and ultimately to the terminal blast phase (BP), resulting in an unfavorable outcome [1–3]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.