The causes of chronic hepatitis include viral hepatitis (HBV and HCV), alcoholic liver disease (ALD), nonalcoholic metabolic disorder-related fatty liver disease (MASH = traditional nonalcoholic steatohepatitis (NASH)), and autoimmune liver diseases (including primary biliary cholangitis (PBC)). Among these, viral hepatitis is particularly serious. As of 2019, the WHO estimated that 296 million people worldwide were chronically infected with HBV and 58 million with HCV, representing approximately 4.4% of the global population. Chronic inflammation due to viral infection leads to gradual liver fibrosis, which can progress to cirrhosis over about 30 years in the case of HCV. Cirrhosis markedly increases the risk of hepatocellular carcinoma (HCC), with approximately 8% of patients diagnosed with HCC each year (Fig. 93.1). For cancer prevention, quantifying the degree of liver fibrosis and promptly eliminating the causative virus upon cirrhosis onset is crucial. Liver fibrosis can be evaluated through physical methods like FibroScan or hematological approaches such as the FIB-4 index, which utilize platelet counts and biomarkers. Biomarkers include fibrotic substances such as hyaluronic acid and collagen, molecules secreted by activated hepatic stellate cells, and proteins expressed by parenchymal liver cells under stress. Changes in glycans on glycoproteins reflect cellular status and serve as excellent biomarkers. One such marker, M2BPGi (Mac-2 binding protein glycosylation isomer), has been approved for in vitro diagnostics [1]. Its cutoff values vary depending on the etiology of fibrosis. Although it shows reduced sensitivity in MASH, it efficiently distinguishes MASLD (metabolic dysfunction-related fatty liver disease = traditional NAFLD) when combined with fucosylated haptoglobin.