We found absence of CD162 alone significantly reduced E-selectin binding potential of murine AML blasts when compared to WT AML blasts (from an average of 65% for WT to less than 4% for Selplg–/– AML blasts binding to E-selectin, p < 0.0001) (Figures 3A–D) which was different from that observed in KG1a cells (previous Figure 1D). The gene discussed is SELE; the disease is acute myeloid leukemia.