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. The gene discussed is FCGR3A; the disease is neoplasm.