This competition allows tumor cells to escape immune surveillance.[16] Lee et al[17] concluded that malignant gliomas were able to escape KLRK1-mediated immune surveillance mainly by suppressing the expression of NKG2DLs, such as MICA and ULBP2, via an autocrine TGF-β loop and MP-dependent cell surface shedding. Here, KLRK1 is linked to malignant glioma.