KLRK1 and neoplasm: Very promising results were obtained in humanized mouse models in which treatment with antibodies that target the site of proteolytic shedding of MIC proteins without affecting their binding to NKG2D resulted in impairment of MIC release from the surface of human tumor cells and, most importantly, in tumor elimination mediated by NK cells through activation of both NKG2D and CD16 [117,118] (Figure 1).