Some drugs, such as histone deacetylase (HDAC) inhibitors or bortezomib, along with conventional treatments such as chemotherapy, radiation therapy, or immunotherapies, combined with NKG2D-blockade therapies, have shown the significant upregulation of NKG2D ligands on tumor cells, by activating the NKG2D+ effector cells that eliminate the tumor [159] (for more key clinical studies, please refer to Table 1). This evidence concerns the gene KLRK1 and neoplasm.