This controversy has been recently clarified by studies that identified NKG2D-MICA/B engagement as a major mechanism of tumor immune surveillance, subverted by tumors through proteolytic shedding of surface MICA/B which at the same time lower membrane-bound MICA/B recognition by NKG2D and induce the saturation of NKG2D with soluble MICA/B [37, 47]. This evidence concerns the gene KLRK1 and neoplasm.