Several immune escape mechanisms sabotaging NKG2D-mediated tumor surveillance have been reported, including down-regulation of NKG2D by cytokines such as TGF-β (18, 20) or tumor-derived soluble NKG2DL (sNKG2DL) as well as of down-regulation of NKG2DL expression by proteolytic shedding, miRNA, or cytokines (20–23). The gene discussed is KLRK1; the disease is neoplasm.