SELE and acute myeloid leukemia: E-selectin is expressed constitutively on specialized marrow microvessels and mediates cell–cell adhesive interactions that create the “vascular hematopoietic niche.” E-selectin is markedly upregulated in the marrow of patients with AML, and there is increasing evidence that E-selectin receptor–ligand interactions induce critical cell survival pathways that mediate AML treatment resistance (18).