KIR3DL1 alleles have been segregated based on patterns of strong (*001, *002), weak (*005, *007) or lack (*004) inhibition by target cells with HLA-B subtypes and in AML patients who received HLA-compatible allografts, donor-recipient KIR3DL1/HLA-B subtype combinations that demonstrate weak or no inhibition were associated with significantly lower relapse and higher survival compared with strong inhibition combinations (Boudreau et al. 2017). This evidence concerns the gene KIR3DL1 and acute myeloid leukemia.