In CML, stromal endothelial cells may further enrich this quiescent phenotype of LSCs by transferring miR-126 to CD34+ CML cells via extracellular vesicles, and the combination of TKI (nilotinib) and an inhibitor of miR-126 (CpG-miR-126) enhances in vivo targeting of CML LSCs [105]. This evidence concerns the gene CD34 and chronic myelogenous leukemia, BCR-ABL1 positive.