In consequence, there must be other factors leading to sufficient AML blast lysis by NK cells [23, 25]. In vivo and also proven in vitro, AML blasts hamper NK cell function by various mechanisms including Treg induction, shedding of soluble NKG2D ligands (MIC and ULBP molecules), and direct cellular interaction inducing unfavorable KIR phenotype and reduction of proactivating NK cell receptors [13]. The gene discussed is KIR3DL1; the disease is acute myeloid leukemia.