In a preclinical model of chronic myeloid leukemia (CML), either sensitive or resistant to the tyrosine kinase inhibitor (TKI) imatinib, directed against the BCR-ABL fusion gene, NSC23766 displayed an antiproliferative effect in vitro and in vivo and blocked malignant cell dissemination in xenograft studies, supporting the notion that during CML pathogenesis, RHO GTPases can be activated by p210-BCR-ABL [136]. This evidence concerns the gene EVPL and chronic myelogenous leukemia, BCR-ABL1 positive.