Of interest, though NK cell induced tumor cell lysis was still lowest in SW480 and HT-29, cetuximab appeared to at least in part bypass the inhibitory effect mediated through NKG2A/HLA-E interactions, probably by tipping the balance of activating and inhibitory signals more towards NK cell activation through binding of cetuximab to the activating FcγRIIIa. This evidence concerns the gene KLRC1 and neoplasm.