Base on NK cell education and “missing-self” recognition, we speculate that mature NK cell subsets that express inhibitory KIR3DL1 for self-HLA-Bw4 ligand may have greater activation potential when the inhibitory signal is interrupted through interactions with HLA-deficient cells such as dysplastic CD34+ cells, which may explain the candidate mechanism of a protective effect on MDS conferred by KIR3DL1-HLA-Bw4 in Chinese Southern Han. The gene discussed is KIR3DL1; the disease is myelodysplastic syndrome.