CML LSCs can be resistant to TKI therapy and remain after therapy, serving as a reservoir for residual disease and relapse due to independent BCR-ABL activity including the various molecular mechanisms and signaling pathways, which are often activated by epigenetic mechanisms and the impact of the bone marrow niche, as mentioned earlier in this study. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.