Therefore, unleashing and harnessing CD56brightNKG2A+ NK cell function by e.g. either by blocking HLA-E on tumor cells, or by blocking NKG2A+ on NK cells or administering cytokines such as IL-15 which expand these NK cell subsets in the patients, might have a strong therapeutic merit in limiting and fighting EBV-associated tumor formation. The gene discussed is KLRC1; the disease is neoplasm.