If the secretion of MICA and MICB by virus-infected or tumor cells is thought to activate the immunological system through the NKG2D receptor on NK and cytotoxic lymphocytes, then the malignant cells may also present this receptor, as hinted in this work, to help deplete the secreted stress signals in situ and thus avoid activation of the cytotoxic NKG2D-positive cells. This evidence concerns the gene KLRK1 and neoplasm.