Under AML stress, several mechanisms involved impairing NK cell function [11]: 1) decreased expression of IFN-γ, TNF-α, NKp30, NKp44, and NKp46, and increased inhibitory NKG2A and KIR2DL2 in NK cells [15–17]; 2) increased AML cell resistance to NK cell-mediated cytotoxicity [18–20]; 3) suppressed by immunosuppressive cell types, such as DC and Treg [21–23]. The gene discussed is NCR2; the disease is acute myeloid leukemia.