Clinically, human studies document reduced NK counts/cytotoxicity in sepsis and up-regulated inhibitory checkpoints (e.g., PD-1/PD-L1, NKG2A), with higher PD-L1+ NK proportions correlating with greater illness severity and poorer short-term outcomes—underscoring a narrow therapeutic window that favors calibrated, context-specific modulation rather than uniform augmentation [69, 72]. The gene discussed is KLRC1; the disease is Sepsis.