Using a CML murine engraftment model, combined E-selectin inhibitor GMI-1217 (uproleselan) and imatinib led to improved survival and reduced BM endothelial adherence, compared to imatinib alone, supporting the hypothesis that E-selectin mediated adhesion by CML LSCs (via CD44) is an imatinib resistance mechanism [45]. Here, CD44 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.