In patients with AML, NK cells are markedly reduced in number and show a dramatic impairment in cytotoxic efficacy due to down-regulation of NK cell-activating receptors [particularly KLRK1 and natural cytotoxicity triggering receptor 1 (NCR1) and 3], defective AML-NK synapse formation, and increased shedding of soluble ligand forms (Costello et al., 2002; Fauriat et al., 2007; Khaznadar et al., 2014; Lichtenegger et al., 2014). The gene discussed is NCR1; the disease is acute myeloid leukemia.