The international medical community has an analogy for the goal of antiviral therapy for chronic hepatitis B: a negative hepatitis B virus DNA is the bronze medal, a serologic conversion of hepatitis B virus e antigen (meaning a negative antigen with the possibility of antibody development, hereafter referred to as “conversion”) is the silver medal, and a negative hepatitis B virus surface antigen is the gold medal. In the past, “winning the gold medal” was considered an “impossible task”, but in recent years, the international medical community has explored the possibility of “winning the gold medal”. A study presented at the 2007 European Liver Conference showed that 116 patients with hepatitis B who were treated with PEG interferon for one year had 4, 7, and 9 hepatitis B surface antigen reversions in the first, second, and third years afterwards, with reversion rates of 3%, 6%, and 8%, respectively. In a study presented at the 2007 American Liver Congress, researchers statistically analyzed 194 patients with chronic hepatitis B who were treated with PEG interferon or PEG interferon plus lamivudine for 48 weeks and followed up for 3 years and found that the quantitative analysis of hepatitis B surface antigen in the blood at 48 weeks of treatment Among the 23 patients with less than 10 international units per milliliter, 12 patients (52%) had a negative surface antigen after 3 years, while among the 171 patients with more than 10 international units per milliliter, 4 patients (2%) had a negative surface antigen after 3 years. Thus, the medical community believes that quantitative hepatitis B surface antigen analysis can be used as a predictor of the likelihood of achieving surface antigen regression in patients with chronic hepatitis B. More encouraging results from recent studies have shown that among patients who experienced HBeAg serologic conversion with interferon therapy, HBsAg clearance occurred in 30% of patients after 3 years of follow-up; 6 years of follow-up showed that HBsAg clearance could be as high as 45%. At 96 weeks of treatment with pegylated interferon, 53% of patients showed HBeAg clearance; at 5 years of follow-up after drug discontinuation, HBsAg clearance could be as high as 72% if the patient’s HBV DNA was consistently <400 copies/ml. Even more promising is the fact that long-term treatment with nucleoside analogs can also result in HBsAg clearance. The clearance rate of HBsAg is significantly increased after treatment with newer and more potent nucleoside analogues such as tenofovir, and recently it was reported that HBsAg clearance rate of 6% was achieved in some subgroups after 1 to 2 years of tenofovir treatment. The author has likewise treated multiple complete conversions in patients and is pleased to see that the percentage of HBsAg clearance after obtaining a durable virologic response increases with longer follow-up in both HBeAg-positive and negative patients. Such results can already be seen as a leap forward compared to the 1%-2% annual natural conversion rate after hepatitis B virus infection, which was unthinkable in the past. Thus, it has been determined that hepatitis B surface antigen reversion in clinical treatment is a goal that can be pursued. Clinicians should strictly control the indications for antiviral therapy, select the right target population and the right drugs, and especially emphasize adequate regimen and full management to avoid unregulated treatment and blind treatment. In other words, the principles of treatment optimization should be implemented, including: (i) patient selection, which allows the selection of patients with good antiviral treatment outcomes through the selection of baseline levels; (ii) drug selection, which must also optimize the selection of antiviral drugs based on the risk-benefit ratio of treatment; and (iii) optimization of efficacy, which can further optimize the outcomes of antiviral treatment through in-treatment monitoring and optimization of treatment regimens. The manifestation and regression of hepatitis B can be very different due to the different immune status, age, lifestyle habits and stage of infection of the patients, some of them just show the status of virus carriage, some have mild liver function abnormalities, some have recurrent attacks with significant liver damage, and some patients even have liver failure or even life-threatening. It is because of these differences that the treatment of hepatitis B must be individualized and tailored to the individual, and the same individual at different stages, the treatment method is not the same, I would like to remind patients not to see others with a good effect of a certain drug, they also blindly try, must be under the guidance of a specialist medication.