This observation, even if as an indirect proof and performed only in a small series of cases, could prompt us to hypothesize that (1) BMI1 is specifically expressed by the CML CD26+ LSC, and (2) because of its BCR-ABL1-independent behavior, BMI1 could be considered as one of the mechanisms of resistance to TKIs, that would make this gene an interesting therapeutic target for new drugs in the CML landscape. This evidence concerns the gene BMI1 and chronic myelogenous leukemia, BCR-ABL1 positive.