Non-alcoholic fatty liver disease is often misunderstood as fatty liver disease caused by non-alcoholic factors. In fact, the common viral hepatitis B and C, or the increasing number of drug-related hepatitis in recent years, as well as hepatomegaly and total parenteral nutrition, also often occur as hepatocellular steatosis, but are not part of NAFLD and are treated differently. NAFLD is almost always accompanied by obesity, diabetes, hypertension, hyperlipidemia, and hyperuricemia. Treating these associated conditions is often more urgent than treating fatty liver itself, as they are the direct cause of life-threatening conditions. Effective treatment of these conditions often helps treat NAFLD as well, but is not a complete substitute for fatty liver treatment. One of the more dangerous types of non-alcoholic fatty liver disease is called Non-Alcoholic Steato Hepatitis (NASH), which is mostly detected incidentally during routine physical examinations. Compared to simple steatohepatitis, patients have more fatigue, vague liver pain, elevated serum transaminases (ALT, AST) and/or transpeptidases (γ-GT), and a slight increase in bilirubin. However, elevated liver enzymes do not correlate positively with the severity of the disease on ultrasound imaging. That is, a “mild fatty liver” on ultrasound does not mean that NASH is not present. The risk of NASH lies in its chronic insidious intrahepatic inflammation causing persistent hepatocellular necrosis and intrahepatic collagen fibrous deposits, with approximately 20% of patients eventually progressing to cirrhosis with serious life-threatening consequences. Therefore, active treatment is necessary. The mechanism of NASH can be briefly described as the metabolic disorder caused by insulin resistance in the patient’s body, which leads to a large amount of free fatty acids from extrahepatic fat, especially white fat, entering the hepatocytes, exceeding the ability of mitochondria in the hepatocytes to metabolize fatty acids and forming a large amount of triglycerides in the hepatocytes, which cannot be discharged from the hepatocytes in time, resulting in fat deposition in the hepatocytes (first strike). This is followed by fat peroxidation stress that damages hepatocytes (second strike). NASH treatment is not simply “eat less and exercise more”. It should be done in two steps. Step 1: Inhibit the acute damage of hepatocytes, including the application of silymarin, reduced glutathione, glycopyrrolate, carnitine orotate, ezetimibe, ursodeoxycholic acid and other drugs to normalize liver enzymes, while resting properly and reducing caloric intake. Fat consumption through vigorous aerobic exercise is not advisable at this stage. Step 2: After the liver enzymes are normal, the patient should be instructed to gradually strengthen aerobic exercise such as jogging, brisk walking, swimming, playing ball, jumping rope, shuttlecock, etc. according to the specific situation, which should be adhered to. At the same time, reduce food consumption and change the ratio of food intake (high protein, low sugar, low fat) in a planned manner to reduce body weight.