SELE and neoplasm: From a therapeutic perspective, 3F-Neu5Ac operates through two critical mechanisms: it inhibits ST3GAL6-catalyzed generation of E-selectin ligands, blocking MM cell homing to BMM and restricting tumor cell entry into drug sanctuaries; simultaneously, it disrupts glycosylation-dependent maturation of integrin α4 chains, directly impairing tumor-stromal cell adhesion-dependent survival signals [133].