For instance, in CML, dissociating the interaction between E-selectin, an adhesion molecule expressed on the endothelial cells within the endosteal BM microenvironment, and CD44 using the E-selectin inhibitor GMI-1271 sabotages BM homing of LSC-enriched CML cells, enhancing CML sensitivity to eradication by TKIs such as imatinib mesylate and prolonging survival of mice with CML [62,63]. The gene discussed is SELE; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.