In addition to the emergence of high percentages of CD56negCD16+ NKs, HCMV infection induces a strong imprinting in the development of NKs not only by accelerating the differentiation of NKG2A-KIR+ NKs, but also by inducing a significant increase in CD56dim NKs expressing the NKG2C receptor together with CD57: the so-called adaptive NKs (11, 12). Here, KIR3DL1 is linked to cytomegalovirus infection.