Imatinib, the first TKI developed, is capable of inducing complete hematologic and cytogenetic response in the majority of chronic-phase CML (CP-CML) patients, and the goal of CML therapy has moved to the achievement of a major molecular response (MMR; defined as BCR::ABL1/ABL1 ratio ≤0.1% on the international scale (IS)) and possibly the achievement of a deep molecular response (DMR; defined as BCR::ABL1/ABL1IS ratio ≤0.01%), which might represent an “operational cure” as well as a prerequisite for treatment discontinuation [1,2]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.