Data derived from in vitro and animal experiment data have indicated that the Fpr2/3 gene (an orthologue to human FPR2/ALX) is crucial to enacting nonredundant functions including control of cell recruitment, phagocytosis, modulation of soluble mediator generation, and containment of bacteremia, which prevents spread to vital organs and opens new opportunities to manipulate the host response in sepsis. The gene discussed is FPR2; the disease is Sepsis.