In primary AML, leukocyte immunoglobulin-like receptor B4 (LILRB4) is highly expressed (its expression level is 40–50 times higher than that of PD-L1 and PD-L2 in AML) and promotes tumor infiltration through suppressing T cell activity and triggering immune evasion beyond PD-L1 and L2. Here, LILRB4 is linked to neoplasm.