In chronic myeloid leukemia (CML), the dormant LSCs are largely independent on the BCR-ABL signaling and therefore cannot be eradicated by BCR-ABL tyrosine kinase inhibitors (TKIs), so that disease often reoccurs upon discontinuation of TKI treatment [14–17]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.