The new populations of tumor variants may eventually evade the immune system and escape from host immune surveillance by a variety of mechanisms including loss of MHC-I, adhesion molecules, tumor-associated antigens (TAAs), generation of regulatory T- (Treg-) lymphocyte, expansion of myeloid-derived suppressor cells (CD11b+ Gr-1+ cells, MDSCs), immunosuppression, blocking of NKG2D-mediated activation, and apoptosis induction of antitumor effector cells [50, 51]. Here, KLRK1 is linked to neoplasm.