Our experiments using mice that are either deficient for the IL-4 receptor alpha, which is required for AAM induction, or deficient for IL-4, which is necessary for the suppressive function of AAM [39, 40], suggest, however, that modulation of NFκB and TLR signaling, but not the induction of an AAM phenotype, improves sepsis outcome in L. sigmodontis-infected mice. The gene discussed is NFKB1; the disease is Sepsis.