Interestingly, in contrast to some in vitro experiments based on co-cultures showing that HLA-E overexpression by CRC cell lines inhibits the cetuximab-mediated cellular cytotoxicity by NK cells via engagement of its inhibitory CD94/NKG2A receptor (8), we failed to demonstrate a negative impact of HLA-E/β2m overexpression by tumor cells or presence of CD94+immune cells on the clinical response to cetuximab. The gene discussed is HLA-E; the disease is colorectal carcinoma.