In a mouse model of obstructive extrahepatic and intrahepatic cholestasis, NGM282 administration inhibited hepatic CYP7A1 expression, thus reducing the concentration of hepatic BAs and serum liver enzymes and preventing cholestatic liver injury.99 In a mouse model of PFIC, NGM282 alleviated liver injury, inflammation, and fibrosis, downregulated the expression of CYP7A1, and reduced BA pool size.100 These results indicate that NGM282 is a promising therapeutic agent for cholestasis. The gene discussed is CYP7A1; the disease is intrahepatic cholestasis.