They (1) physically shield CTCs from immune recognition [90], (2) secrete immunosuppressive factors including TGF-β [91], (3) transfer MHC class I molecules to cancer cells to establish a state of pseudo-self-tolerance [92], (4) induce the shedding of NKG2D ligands [93], and (5) express NK cell inhibitory ligands such as glucocorticoid-induced TNF-related ligand (GITRL) [94]. This evidence concerns the gene KLRK1 and cancer.