In line with previous reports, infection with human cytomegalovirus (HCMV)—which induces the expansion of highly differentiated CD57+ and NKG2C+ NK cell populations with an “adaptive” (FcεR1γ−) phenotype and specialised towards antibody-dependent responses19,20—was a significant modifier of the ADCC response to EBOV GP. The gene discussed is KLRC2; the disease is infection.