1.Pathological diagnostic criteria: HCC is diagnosed by pathological histological and/or cytological examination of biopsy or surgical resection of tissue specimens from occupying liver lesions or extrahepatic metastases, which is the gold standard. 2.Clinical diagnostic criteria: Among all solid tumors, only HCC can be diagnosed by clinical diagnostic criteria, which are recognized both domestically and externally as non-invasive, easy, convenient and operable, and are generally considered to depend mainly on three major factors, namely chronic liver disease background, imaging findings and serum AFP level. However, the understanding and specific requirements of the academic community are different and often change, and there are errors in the practical application. (1) evidence of cirrhosis and HBV and/or HCV infection (positive HBV and/or HCV antigen); (2) typical imaging features of HCC: simultaneous multi-row CT scan and/or dynamic contrast-enhanced MRI showing rapid inhomogeneous vascular enhancement of the hepatic occupancy in the arterial phase with venous or delayed phase Rapidly eluting. (1) If the diameter of liver occupancy is ≥2 cm, one of the two imaging examinations of CT and MRI shows that the liver occupancy has the features of hepatocellular carcinoma mentioned above, HCC can be diagnosed; (2) If the diameter of liver occupancy is 1-2 cm, both imaging examinations of CT and MRI need to show that the liver occupancy has the features of hepatocellular carcinoma mentioned above before HCC can be diagnosed to enhance the specificity of diagnosis. (3) Serum AFP ≥ 400 μg/L for 1 month or ≥ 200 μg/L for 2 months, and other causes of elevated AFP can be excluded, including pregnancy, germline embryonic-derived tumors, active liver disease and secondary liver cancer. (1) Several foreign guidelines (including AASLD, EASL and NCCN’s CPGs) emphasize that multi-row CT scans and/or dynamic contrast-enhanced MRI should be performed at experienced imaging centers for hepatic occurrences; at the same time, it is believed that a definitive imaging diagnosis of HCC requires a four-phase scan of the plain, arterial, venous and delayed phases. HCC is characterized by an early arterial phase with significant enhancement and higher density than normal liver tissue, and a venous phase with rapid loss of enhancement and lower density than surrounding normal liver tissue. If the imaging features of liver occupancy are atypical, or the two CT and MRI examinations are inconsistent, liver puncture biopsy should be performed, but even if the negative result does not completely exclude, follow-up observation is still needed. (2) In recent years, clinical observations and research results at home and abroad have suggested that serum AFP can also be elevated in some patients with ICC and liver metastases from gastrointestinal cancer, and ICC is also mostly accompanied by cirrhosis. Although the incidence of ICC is much lower than that of HCC, both are commonly seen in patients with cirrhosis, therefore, liver-occupying lesions with elevated AFP are not necessarily HCC and need to be carefully differentiated. In China and most countries in the Asia-Pacific region, patients with significantly elevated AFP are more likely to have HCC, which still has a differential value compared with ICC, and is therefore used here as a diagnostic index for HCC. (3) For those with serum AFP ≥ 400 μg/L and no liver occupancy detected by ultrasound, attention should be paid to exclude pregnancy, germline embryonic-derived tumors, active liver disease and gastrointestinal liver-like adenocarcinoma; if it can be excluded, multi-row CT and/or dynamic contrast-enhanced MRI scan must be performed promptly. The diagnosis of HCC is made if typical HCC imaging features are presented (rich vascularity in the arterial phase with regression in the portal or delayed phase.) If the findings or vascularity are not typical, contrast-enhanced examination with other imaging modalities or liver biopsy of the lesion should be performed. Arterial phase enhancement alone without venous phase regression is not sufficient evidence for the diagnosis of HCC. If AFP is elevated but not at diagnostic levels, in addition to the above-mentioned conditions that may cause AFP elevation should be ruled out, it is important to closely observe and follow the changes in AFP by reducing the ultrasound interval to 1-2 months and performing CT and/or MRI dynamic observation when needed. If hepatocellular carcinoma is highly suspected, further selective hepatic arteriography (DSA) is recommended, and liver aspiration biopsy may be performed if necessary and appropriate. (4) For those with hepatic occupying lesions but no elevated serum AFP and no imaging features of hepatocellular carcinoma on imaging, if the diameter is <1 cm, close observation can be performed. If no vascular enhancement is seen in dynamic imaging of the liver occupancy, malignancy is unlikely. If the occupancy gradually increases or reaches ≥2 cm in diameter, further examination such as ultrasound-guided liver aspiration biopsy should be performed. Even if the liver biopsy result is negative, it should not be easily dismissed and should be followed up; imaging follow-up should be performed at 6-month intervals until the lesion disappears, increases in size, or presents diagnostic features of HCC; if the lesion increases in size but still does not have typical HCC changes, repeat liver biopsy can be considered. (5) It should be noted that 5%-20% of patients with HCC in China do not have a background of cirrhosis, about 10% have no evidence of HBV/HCV infection, and about 30% have serum AFP consistently <200 μg/L; meanwhile, most of the imaging HCC has features of rich vascularity, but a few do show lack of vascularity. In addition, in Europe and the United States, patients with nonalcoholic steatohepatitis (NASH) can develop cirrhosis and then HCC (NASH-associated HCC), which has been reported more frequently, while there is a lack of relevant data in China.