However, in spite of continuous TKI administration, a large majority of CML patients persistently display measurable residual disease and cannot stop their treatment without signs of relapse [4], reflecting the relative insensitivity of residual CML stem/progenitor cells to TKIs despite efficient inhibition of BCR-ABL1 activity [1, 2]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.