In line with the relevance of NKG2D/NKG2D-L interaction in tumor control there is the recent observation that gastric circulating tumor cells (CTC) undergoing epithelial to mesenchymal transition (EMT) downregulate ULBP1 [139], thus possibly favoring metastatic growth by evading NK-mediated killing. Here, KLRK1 is linked to neoplasm.