KLRK1 and neoplasm: While most of the studies with human NKG2D ligands demonstrated that soluble NKG2D ligands suppress tumor immunity [29,37,38,39], controversy arose from findings that the overexpressing of soluble mouse NKG2D ligand, sMULT-1, in B16F10 tumor cells resulted in no tumor formation [32], suggesting that the role of soluble NKG2D ligands in regulating tumor immunity could be more complicated than what has been understood to date.