KLRK1 and neoplasm: A drastic downregulation of NKG2D at the tumour site alludes to two possibilities: one, that the reduction of NKG2D expression is a result of NK cell exhaustion, wherein tumour-infiltrating NK cells have long been functionally impaired as a result of chronic overstimulation [85,86], or two—MBLs have successfully co-opted a different molecular mechanism to abrogate NK cell activity.