In CML, for example, the rearrangement of BCR and ABL1 genes gives origin to a fusion gene where the control of the ABL1 kinase function is lost and so the new protein is constitutively active, with the consequent excess of proliferation of myeloid precursors and an abnormal interaction of the leukemic stem cells with the actin and the bone marrow stroma (69) (Figure 2, left hand panel). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.