If these results are confirmed in clinical settings, cholestatic patients with endotoxemia, and potentially those with other inflammatory cholestatic diseases, may benefit from the well-established anti-inflammatory effects of OCA, its FXR-mediated regulation of hepatocellular transporter expression, and possibly from signaling mechanisms that ensure appropriate localization of newly synthesized transporters, thereby preventing excessive degradation. The gene discussed is NR1H4; the disease is serum lipopolysaccharide activity.