Further consideration deserves the role of AURKA, PLK1 and FOXM1 in the persistence of LSC, representing, so far, the major limitation to CML cure In particular, FOXM1 inhibition may revoke its ability of conferring stem-like properties to transformed cells either directly or through AURKA recruitment in the nuclear compartment, hence supporting the advantage of specific inhibitors as complementary drugs to deplete the LSC pool [46–51]. The gene discussed is AURKA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.