The process of liver fibrosis formation is generally speaking not complicated, when the liver is damaged, causing inflammation and necrosis of hepatocytes, activating hepatic stellate cells, producing a large amount of extracellular matrix and forming liver fibrosis. To put it simply, this process is in fact a very complex one, and understanding continues to advance with advances in molecular biology research. The causes of liver damage are diverse and common factors include: infectious (e.g. HBV,HCV, etc.), chemical toxic (ethanol and drugs), autoimmune, cholestatic, metabolic and congenital. Such as our most common diseases: chronic hepatitis B and C, alcoholic and non-alcoholic fatty liver, etc. Liver fibrosis is mostly seen in chronic liver disease, this is because acute inflammation of the liver also leads to a decrease in the number of hepatocytes and fibrous proliferation, but the hepatocytes can be restored by repair and regenerative functions. At the same time, the fibrous components that have been produced can be degraded and removed, restoring the composition and structure within the liver tissue to normal and therefore not producing liver fibrosis. Only in various chronic liver diseases, persistent or repeated inflammatory necrosis of hepatocytes leads to an enhanced repair response of the organism and massive fiber proliferation, while the relative or absolute deficiency of fiber degradation causes massive deposition of fibrous material and the formation of hepatic fibrosis. People’s understanding of liver fibrosis has gone through three stages. In the first stage, it was thought that liver fibrosis was static, a post-inflammatory repair response, like a scar after a skin injury that cannot disappear. In the second stage, it was recognized that liver fibrosis is a dynamic process, and that whether liver fibrosis occurs and whether it progresses or subsides depends on the relative activity of extracellular matrix synthesis and degradation (fibrous proliferation or breakdown). It is no longer believed that liver fibrosis is irreversible, but it is recognized that aggressive treatment during the fibrosis stage can effectively prevent or delay the formation of cirrhosis. In the third stage, people began to look for effective anti-fibrotic treatments at the level of cytokines, signaling, and gene regulation on the basis of cellular and molecular biology. The difference between liver fibrosis and cirrhosis There is a qualitative difference between liver fibrosis and cirrhosis. Liver fibrosis is an intermediate stage in the evolution of chronic liver disease into cirrhosis, a continuous progression in the evolution of the disease, and it is difficult to separate the two clinically. Strictly speaking, liver fibrosis is a pathological concept, while cirrhosis is the clinical diagnosis of a chronic disease. The difference between the two is that clinically there are no specific signs and symptoms of liver fibrosis, while cirrhosis has a clinical diagnosis and diagnostic indicators in the form of ancillary tests. Liver fibrosis can be reversed with treatment, while anti-fibrotic treatment for mid- to late-stage cirrhosis is less effective. The development of cirrhosis must go through three basic stages: first, repeated inflammation and necrosis of hepatocytes, and second, the formation of liver fibrosis, where fiber proliferation is much greater than decomposition. The third is the generation of regenerative nodules of hepatocytes, the formation of pseudobullets and the gradual loss of function. The formation and progression of liver fibrosis often occurs quietly in the clinic, and the disease is insidious and not easily detected and taken seriously. A study conducted by experts found that 22% of asymptomatic carriers of hepatitis B virus with normal liver function had active inflammation of the liver, and 40% of them had cirrhosis. Therefore, the early diagnosis and effective treatment of liver fibrosis is a key link in the prevention and treatment of liver cirrhosis.