Intestinal inflammation was positively affected by lipid signaling, microbial changes, and AA accumulation in both animal models, pointing to a shared molecular mechanism which involved RXR binding, activation of PPARs, and FXR competition.50 Therefore, our findings may open therapeutic horizons in treating cholestatic liver diseases such as PSC through the gut–liver axis, suggesting the potential for selective MGL antagonists as a future treatment strategy. The gene discussed is MGLL; the disease is liver disorder.