In a human study of intensive care unit participants, the killer cell Ig-like receptor-3DL1 (CD158e), an inhibitory NKR, was significantly higher in the sepsis group than in the systemic inflammatory response syndrome group; however, other activating or inhibitory NKRs, including NKp30, NKp46, and NKG2A/C/D, were similar between the two groups [20]. This evidence concerns the gene KLRC1 and Sepsis.