The formation of a terminally differentiated NK cell subset (NKG2a/clowCD16+) with robust innate and adaptive antiviral activities, which was found in nonpathogenic infections in AGMs7, was blocked in pathogenic SIVmac infection in favor of intermediate differentiation (NKG2a/chighCD16+) with heightened pro-inflammatory potential36. Here, KLRC1 is linked to infection.