KLRK1 and neoplasm: Together, these data suggested that: (1) tumor-infiltrating NK cells are engaged by non-tumor RAE-1ε; (2) nonhematopoietic cells are the primary endogenous source of RAE-1ε responsible for NKG2D engagement; and (3) endothelial cells in transplanted tumors and autochthonous models of mouse cancer are induced to express especially high amounts of RAE-1ε.