These receptor-level disparities help explain the apparent paradox that human NK cell deficiencies are associated with severe infection and higher mortality, whereas selected murine settings report survival benefits from NK/effector attenuation (e.g., granzyme A deficiency or inhibition) during abdominal sepsis—differences likely reflecting immune system complexity, lifelong microbial exposures, immunosenescence, and phase-dependent NK effects [80]. The gene discussed is GZMA; the disease is hyperinsulinemic hypoglycemia, familial, 4.