In addition to angiogenesis enhancement that tumor-EV promote in CML, MV from the CML cell line K562 may transfer the BCR-ABL1 mRNA to normal BM-MSC and induce BCR-ABL1 ectopic expression, leading to exacerbated MSC proliferation and TGF-β1 secretion, without cytogenetic abnormality (Figure 4) [84]. This evidence concerns the gene TGFB1 and chronic myelogenous leukemia, BCR-ABL1 positive.