For instance, PPAR‐targeting drugs are shown to reduce hepatic steatosis, lobular inflammation and hepatocellular ballooning in nondiabetic MASH subjects.[38] Farnesoid X receptor agonists reduce bile acid synthesis and improve hepatic steatosis and damage.[39] However, the effectiveness of these drugs is often limited by adverse events and other concomitant metabolic disorders.[38, 39] These limitations strongly suggest that alternate medications with improved efficacy and safety are critically needed. The gene discussed is PPARA; the disease is fatty liver disease.