The involvement of Fprs in mouse resistance to Listeria infection was further indicated by the ability of Listeria to produce chemotactic agonists for both Fpr1 and Fpr2 (38) and while mice deficient in a single Fpr showed increased bacterial load in the liver, deficient in both Fpr1 and Fpr2 resulted in greater bacterial load in the liver and animal mortality after infection. The gene discussed is FPR2; the disease is infection.