These authors also show that the aggressive tumours developed in NKG2D-deficient mice express higher levels of NKG2D ligands (which mediate NK-mediated destruction of some tumour cells) than the tumour cells from wild-type mice, suggesting that in immunocompetent mice one of the early events in the immunoediting of spontaneous tumours may be the selection of tumour-cell variants that express low levels of NKG2D ligands. The gene discussed is KLRK1; the disease is neoplasm.