Given that HCMV infection induces a highly differentiated phenotype within the CD56dim subset we assessed the surface expression of NKG2C/A, KIRs (focusing on mainly in inhibitory KIRs using a cocktail of antibodies against KIR2DL1/S5, KIR2DL2/L3/S2, KIR3DL2, and KIR3DL1), CD85j/LIR-1 and the terminal differentiation marker CD57 on this subset in relation to HCMV serostatus in the entire study cohort. The gene discussed is LILRB1; the disease is cytomegalovirus infection.