The importance of the in vivo testing of such hypothetical models of NKG2D immune escape was highlighted by the recent study from the Raulet laboratory where, contrary to current belief, release of a soluble NKG2DL by B16 tumor cells did not impair NK cell functions and tumor rejection, but rather resulted in an enhanced NK cell reactivity and faster tumor rejection (51). This evidence concerns the gene KLRK1 and neoplasm.