The expansion of a “clonal” NKG2C+ NK cell subset was also identified as the major reason for perturbations of the KIR repertoire; in human CMV infection, strong NKG2C+ NK-cell expansion is dominated by a single inhibitory KIR clone, whereas moderate expansion is more frequently polyclonal (Manser et al., 2019). Here, KIR3DL1 is linked to cytomegalovirus infection.