Chronic hepatitis B is a disease that causes inflammatory damage to the liver as a result of infection with the hepatitis B virus. China has a large number of patients with slow hepatitis B, and is the so-called hepatitis B country. Many people think that once they have slow hepatitis B, it will never be cured and will develop into cirrhosis and liver cancer, so they are inevitably worried about it all day long. In fact, this concept is one-sided, hepatitis B is indeed bad treatment, with the development of medical technology, we can effectively control the hepatitis B virus replication, slow down the progress of the disease, reduce the occurrence of cirrhosis, liver cancer, and may even cure some hepatitis B patients. Therefore, we should be more concerned about how to treat slow hepatitis B in order to have better results. What are the criteria for good outcomes in the treatment of slow hepatitis B? Doctors usually use the occurrence of a “response” to evaluate whether an antiviral drug is effective. Antivirals may produce a variety of responses: a biochemical response in the form of normal ALT, a virological response in the form of decreased or negative HBV DNA, and a serologic response in the form of HBeAg and HBsAg clearance or seroconversion. All these responses help to reduce the occurrence of cirrhosis and hepatocellular carcinoma. Compared with other responses, serologic responses can further delay disease progression, although they are also more difficult to obtain. In addition, the efficacy of the drug should be judged from the time dimension. If the above response can be maintained after stopping the treatment, it is called “durable response”. The EASL guidelines, the definitive guideline for chronic hepatitis B, also emphasize that treatment of chronic hepatitis B should aim for durable response after discontinuation, not just during treatment. How can treatment achieve a durable response after discontinuation? The key is immune control, and to achieve this goal, treatment should focus on both suppressing the virus and improving the body’s immunity. Compared to nucleoside analogs with direct antiviral effects, pegylated interferon not only suppresses the virus, but also controls hepatitis B virus infection through immune-mediated control, allowing patients to achieve higher HBeAg serological conversion rates, longer-lasting responses after drug discontinuation, and a sustained reduction in the risk of cirrhosis and hepatocellular carcinoma. Studies have shown that HBeAg serologic conversion rates are high with pegylated interferon alpha-2a treatment and continue to increase after the end of treatment, with up to approximately 60% of patients achieving HBeAg serologic conversion six months after discontinuation. HBeAg seroconversion with pegylated interferon alpha-2a has good durability, with nearly 90% of those patients who achieve HBeAg seroconversion six months after discontinuation continuing to do so one year after discontinuation. In conclusion, slow hepatitis B can be effectively treated, and scientific use of medication has the opportunity to achieve a durable response after drug discontinuation, allowing the disease to go into full remission for a long time to come and no longer require treatment.