Moreover, other TLR agonists (e.g. LPS), cytokines (e.g. IFN-α, IL-15) or parasite infection, stimulated macrophages or DCs were also found to activate NK cells by increasing expression of NKG2D ligands, and thus augment NK cell-mediated cytotoxicity to tumor or infected cells [19], [30], [31], [32], [33]. This evidence concerns the gene KLRK1 and neoplasm.