While lifestyle improvements are the most safe and reliable treatment for NAFLD, researchers have not stopped exploring pharmacological treatments. The results of two recent high level evidence-based studies on vitamin E for NAFLD were published in the New England Journal of Medicine and the Journal of the American Medical Association (PAMA), respectively. The results showed that the vitamin E group showed a significant improvement in liver histology compared to the placebo group (43% vs. 19%), while a partial treatment effect was observed in the pioglitazone group but was not significant compared to the placebo group. Another similar study (TONIC), conducted over 5 years, enrolled 173 underage patients with NAFLD who were randomized to vitamin E, metformin (a diabetic drug), and placebo, and found that after 96 weeks of treatment, the vitamin E-treated group showed a significant improvement in some histologic parameters such as hepatocellular ballooning score (p=1), although the vitamin E-treated group showed a significant improvement in the hepatocellular ballooning score (p=1). ballooning score) (p=0.006) and NAFLD activity score (p=0.02), there was no significant difference in other histological indicators and observations such as liver enzymology. The seemingly opposite findings of the two studies make the future of vitamin E for fatty liver confusing, but analyzing the details of the two studies, it is easy to see that this difference may be due to their slightly different trial designs. First, PIVENS was conducted in adult patients with NAFLD without diabetes, while TONIC enrolled minors (7-17 years old) with NAFLD. In addition, in terms of primary study indicators, compared to PIVENS, which used liver histological changes as the primary study indicator, the TONIC study used liver function indicators such as transaminases as the primary study observation data. In its analysis of histological specimens, the trial found that although no significant improvement was seen in pathological indicators such as liver fibrosis, the vitamin E-treated group had two pathology scores that evaluated the degree of inflammatory lesions The group had an advantage. Based on the results of these two studies, the 2012 U.S. guidelines for the treatment of nonalcoholic fatty liver disease recommended Vit E (800 IU Qd) for improving liver histological damage in adult NASH patients without diabetes and recommended Vit E as the drug of choice for adult NASH patients without diabetes. In contrast, both studies failed to confirm that vitamin E reverses liver fibrosis, so it is not recommended in the guidelines as a therapeutic agent for fatty cirrhosis either. It should be noted, however, that in both the PIVENS and TONIC studies, vitamin E was administered for up to 96 weeks, meaning that high doses of vitamin E were required over a long period of time to reduce steatosis in the liver, and while it is understandable that histological improvement takes time, long-term use of a drug, even a vitamin class, may expose the user to certain other risks. Vitamin E, once the star product against oxidative stress, was popular in Europe and the United States and was believed by people and even some doctors to have cosmetic and age-delaying effects, but after decades of popularity, several epidemiological studies have found that antioxidant supplementation is not as rosy as initially believed. Although there is a debate in the academic community as to whether high doses of vitamin E over time lead to an increase in all-cause mortality, several studies have confirmed that high vitamin E supplementation in healthy people increases the risk of exposure to tumors such as prostate and breast cancers. Therefore, for patients with NASH to be treated with vitamin E, it is important to adequately assess the risks, such as screening for the risk of gonadal tumors before administration, and to inform patients so that they can anticipate the course of the drug. Furthermore, as seen in the TONIC study, although vitamin E may improve inflammatory damage in NASH, this improvement may not be consistent with a decrease in transaminases, or the effect of treatment cannot be judged simply by changes in liver enzymes. Any drug is a double-edged sword, and the treatment process needs to be adjusted from person to person. For fatty liver patients, the best way is still to move and a complete change of bad habits is the best choice.