Only recently, a study showed that in vivo overexpression of Rae-1 on CD11chigh cells, comprising mainly DCs in mice, led to reduced NK cell-mediated cytotoxicity toward NKG2DL+ or MHC class I-deficient targets, compromising the ability of these animals to reject NKG2DL-expressing tumor cells, while the control of viral infection (MCMV) remained unaffected (94). The gene discussed is RAE1; the disease is neoplasm.