Given the potent anti-inflammatory effect of nFhGST on murine macrophages in vitro and endotoxemia in vivo, we hypothesized that nFhGST could be exerting an antagonist effect on TLR-4-signaling consequently altering LPS-induced NF-κB activation and suppressing the production of pro-inflammatory cytokines. This evidence concerns the gene TLR4 and serum lipopolysaccharide activity.