The concomitant reductions in endotoxemia (Figure 1B) and hepatic and Kupffer cell expression of TLR4 (Supplemental Figure S5) and TLR4 targets, including TNF-α (Figures 3I–L, 3U), in the livers of EtOH + Fen-treated mice could provide mechanistic insights into Fen’s mitigation of hepatic steatosis and liver injury, as LPS is a potent stimulator of the TLR4 inflammatory axis (Uematsu and Akira, 2006). The gene discussed is TLR4; the disease is serum lipopolysaccharide activity.