Moreover, LTA4H inhibition shunts LTA4 conversion to the specialized pro‐resolving mediator lipoxin A4 (LXA4)[22] which was found to promote resolution of hepatic inflammation and diminish fibrotic changes in the setting of NASH.[23] Additionally, LXA4 and LTB4 are linked to cholesterol biosynthesis[24] indicating potential synergy with FXR ligands since FXR is the master regulator of bile acid biosynthesis from cholesterol.[14]. The gene discussed is LTA4H; the disease is metabolic dysfunction-associated steatohepatitis.