These results notably demonstrate that although NKG2D-independent NK cell function is intact in the CD11c-Rae1 mice, NK cell–mediated lysis and tumor rejection using three different NKG2D ligand–bearing tumor cell lines are dramatically diminished when DCs constitutively express the NKG2D ligand Rae-1ε, but this functional impairment is reversible. Here, ITGAX is linked to neoplasm.