In the case of myeloid malignancies, chronic myeloid leukemia (CML) cells activate MSCs through soluble factors like CC motif ligand 3 (CCL3) or TPO, and by direct cell-cell contact causing overproduction of functionally altered OBs that do not support normal HSC maintenance [47]. This evidence concerns the gene CCL3 and chronic myelogenous leukemia, BCR-ABL1 positive.