Blocking this interaction with an anti–human CD6 monoclonal antibody resulted in the enhanced killing of tumor cell lines in vitro by NK and CD8+ T-cells mostly via upregulation of the activating receptor NKG2D and increased expression levels of perforin/Granzyme B in parallel with a reduction of the inhibitory NKG2A receptor [55]. Here, KLRK1 is linked to neoplasm.