Using Selplg–/– mice we have previously shown that CD162 was redundant for E-selectin-mediated adhesion of murine HSCs (Winkler et al., 2004, 2012); in contrast we now report that CD162 is critical for adhesion and binding of murine AML blasts to E-selectin. The gene discussed is SELPLG; the disease is acute myeloid leukemia.