Alternatively, Aurora kinase inhibitors have been demonstrated to reduce proliferation, viability and clonogenicity in a CSF3R T618I cell line, similar to their effects in BCR-ABL1-mediated CML and JAK2V617-mediated MPN providing an alternative therapeutic avenue to pursue [127]. Here, CSF3R is linked to chronic myelogenous leukemia, BCR-ABL1 positive.