They showed that in vitro SETBP1 overexpression could efficiently immortalize myeloid progenitors and sustain self-renewal; in mice, SETBP1 cooperated with BCR-ABL1 in transforming committed myeloid progenitors, that normally lack a self-renewal capability, into LSCs, causing the development of myeloid blast crisis of chronic myeloid leukemia (CML). Here, SETBP1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.