Using this in vitro infection, neutrophils from mice deficient in TLR2, NOD2 or FPR1 produced significantly less IL-1β protein (40, 43 and 37 percent decrease, respectively) in response to S. aureus (Fig. 6A), suggesting that activation of TLR2, NOD2 and FPR1 promoted neutrophil production of IL-1β. The gene discussed is FPR1; the disease is infection.