In a more recent study, Lu et al. (99) demonstrated that antibody blockade of soluble MIC in a model of adenocarcinoma could potentiate IFNγ production upon stimulation (100) As elevated levels of soluble NKG2D ligands in the plasma of patients with MM, acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), Hodgkin’s lymphoma (HL), and non-HL have been observed (101–105), it is predicted that NKG2D-expressing iNKT cells will be dysregulated in these tumor microenvironments. This evidence concerns the gene KLRK1 and Miyoshi myopathy.