Therapeutically, the duality of NK biology argues for phase-specific interventions—tempering excessive early NK-driven inflammation, while restoring later NK competence (e.g., judicious IL-15—based support or checkpoint modulation such as PD-1/PD-L1 or NKG2A blockade)—with careful attention to timing, endotype, and pathogen/context, and to translational limits between murine CLP and heterogeneous human sepsis [73–77]. The gene discussed is IL15; the disease is Sepsis.