Primary hepatic carcinoma (PHC) is one of the top 10 malignant tumors published by the World Health Organization, accounting for about 5.4% of new cases and deaths of all malignant tumors worldwide each year. The latest epidemiological findings show that its incidence and mortality are on the rise. Primary hepatocellular carcinoma is a malignant tumor closely related to inflammation, and inflammation has a facilitating role in the development and metastasis of hepatocellular carcinoma. Rudolph Virchow first proposed that inflammation plays a role in the progression of malignant tumors, suggesting that chronic inflammation can promote tumor growth; then Wiemann B demonstrated that acute inflammation caused by injecting patients with Streptococcus pyogenes and Serratia marcescens can degenerate malignant tumors in some patients. The research on the relationship between inflammation and tumor is now a hot topic. A large number of epidemiological investigations suggest that inflammation is one of the most important factors leading to tumorigenesis or promoting tumor development, and about 20% of malignant tumors are induced or promoted by inflammation. Inflammation is associated with multiple aspects of tumor development, including tumor cell formation, progression, escape, proliferation, infiltration, angiogenesis, and metastasis. The molecular and cellular mechanisms by which inflammation causes malignancy are not fully understood. It has been suggested that: after inflammation occurs, inflammatory cells produce large amounts of reactive oxygen and reactive nitrogen species during their migration to the inflammatory site, and the inhibitory effect of endogenous antioxidant mechanisms during chronic inflammation can also produce an overload of reactive substances, which induce DNA damage and disrupt the genetic stability of proliferating cells. Eventually, with repeated damage by inflammation and reactive substances, cellular genetic alterations, including point mutations, gene deletions, and gene recombination, occur. In China, about 1/3 of primary liver cancer patients have a clear history of viral hepatitis B. In Europe, America and Japan, liver cancer is mainly associated with hepatitis C virus infection and alcoholic liver disease. The relationship between hepatocellular carcinoma and hepatitis virus and alcoholic liver disease has been studied extensively at home and abroad, and some of the mechanisms have been elucidated. Studies have confirmed that: hepatitis B virus (HBV) is a DNA virus, which can integrate and insert into the host genome and change the expression of host somatic cell genes, leading to instability of the host cell genome and susceptibility to genetic changes, thus transforming into hepatocellular carcinoma cells; hepatitis C virus (HCV) is a single-stranded RNA virus, which can act with a variety of cellular proteins and promote the transformation of hepatocytes into hepatocellular carcinoma cells. Alcoholic liver disease induces liver cancer formation in which the alcohol product acetaldehyde can directly damage hepatocytes or the reactive oxidants and lipid peroxides produced by ethanol metabolism directly cause DNA damage. Primary liver cancer usually occurs on the basis of chronic liver injury, including chronic hepatitis and cirrhosis, and these are considered precancerous lesions. The inflammatory response caused by chronic liver injury promotes the development of cirrhosis and activates the regenerative capacity of hepatocytes. The structure and function of the liver can be rapidly restored if the repair mechanisms of the liver are transiently activated. The continued activation of repair mechanisms can promote the formation and development of hepatocellular carcinoma, and hepatitis virus infection and chronic alcohol consumption can activate innate immune function and maintain a persistent inflammatory response, thus promoting the formation and development of hepatocellular carcinoma. Current studies have demonstrated the important role of many inflammatory mediators in the relationship between inflammation and cancer. Inflammatory mediators are produced during the inflammatory response and can also be produced by tumor cells. Inflammatory mediators that play a key role include cyclooxygenase-2 (Cox-2), nuclear transcription factor-kappaB (NF-kB), tumor necrosis factor (TNF-α), and the complement system… Primary liver cancer and Cox-2 cyclooxygenase (Cox) is the rate-limiting enzyme for the conversion of arachidonic acid into prostaglandins, also known as prostaglandin endoperoxide synthase, an integral membrane-bound protein with at least three forms: Cox-1 is located in the endoplasmic reticulum and is a structural gene, expressed in a variety of normal tissues and cells, maintaining normal cellular Cox-2 is mainly located in the nuclear membrane and belongs to the inducible type, which is not expressed at rest, but can be rapidly expressed under the stimulation of various inducible factors such as cytokines, hormones and carcinogens, participating in a variety of pathophysiological processes; Cox-3 is transformed from Cox-1 and is only expressed in a few tissues. Recent studies have shown that Cox-2 is not only related to a variety of pathophysiological processes, but also has a close relationship with tumor development. Melchiorre Cervello demonstrated by immunohistochemistry that Cox-2 expression was higher in paraneoplastic tissues than in tumor tissues, and higher in highly differentiated hepatocellular carcinoma than in poorly differentiated hepatocellular carcinoma, and that the expression level of Cox-2 in hepatocellular carcinoma cells decreased with tumor progression, suggesting a role for Cox-2 in early carcinogenesis. The expression level of Cox-2 in hepatocellular carcinoma cells decreased with tumor progression, suggesting that Cox-2 plays a role in early carcinogenesis. Most scholars and research institutions hold the same view. However, there are also different voices. Professor Terence C argues that the expression of Cox-2 in primary hepatocellular carcinoma is not significantly different from the degree of tumor differentiation and significantly different from the TMN stage of the tumor. Cox-2 is closely related to tumor angiogenesis. Angiogenesis has an important role in tumorigenesis and development. In early studies, Cox-2 was thought to have angiogenic properties, but recent studies have demonstrated that Cox-2 may promote tumor angiogenesis by regulating the expression of VEGF and play an important role in tumor invasion. We observed in our experiment (results not yet published) that the expression of both Cox-2 and vascular endotheliogenic factor (VEGF) was increased in primary liver cancer tissues, and they were positively correlated.Cao Bin demonstrated in nude mice that interferon (IFN-α-2b) induced apoptosis and inhibited hepatocellular carcinoma growth by downregulating Cox-2 and VEGF expression water, and suggested that Cox- 2 affects the expression level of VEGF. Compared with normal radiation therapy, body gamma knife has higher precision and less exposure to normal tissues, which can maximize the lesion area to receive high dose and kill tumor cells while reducing the damage to surrounding tissues, and can achieve the purpose of radiation therapy with high dose, high precision, high efficacy and low damage. For patients with primary hepatic cancer (PHC), gamma knife treatment can improve the local control rate and survival rate of PHC. The authors reviewed and analyzed the recent efficacy of body gamma knife treatment in 52 patients with PHC to explore the prognostic factors affecting the treatment and to provide a basis for further clinical application. For the treatment of PHC, surgery is the preferred method, but surgery is only suitable for patients with stage I or II PLC, poor liver function, or when the tumor is adjacent to important structures (portal vein, inferior vena cava, etc.) that cannot be surgically removed, arterial catheter chemoembolization (TACE) or radiotherapy is mostly used as the main treatment. The new generation of radiotherapy technology represented by stereotactic radiotherapy is gradually adopted by radiotherapists because of its high precision, high dose and low damage characteristics. Mornex et al. did a similar study to Park, using a mean radiation dose of 66.0 Gy, resulting in a tumor suppression rate of 91.0% in patients, which shows that the recent efficacy of stereotactic radiotherapy for PHC is remarkable. Body Gamma Knife is a special technique of stereotactic radiotherapy, which can make the shape of the dose distribution in the high dose area consistent with the shape of the tumor target area in the three-dimensional direction during the treatment process, with higher radiation dose in the tumor and less change in the dose gradient, and rapid decrease in the dose outside the tumor, which can increase the radiation dose to the tumor tissue while minimizing the amount of normal tissue exposure, thus improving the local control rate of the tumor. The radiation damage to normal tissues in the early and late stages decreases and improves the quality of survival of patients. Body Gamma Knife uses the head rotation technology to geometrically focus the gamma rays emitted by 60Co in space, so that the high dose of gamma rays is concentrated in the lesion area, while the dose of surrounding normal tissues is sharply reduced, thus achieving the purpose of tumor control without causing significant normal tissue damage. Body gamma knife has the following characteristics: ① can achieve the treatment area conformal and intensity adjustment, the surrounding key organs can be better protected; ② large treatment range, for tumor diameter greater than 15cm can be implemented; ③ for multiple lesions can be treated at the same time; ④ using a higher fraction of the dose, biological killing effect is obvious. Body Gamma Knife for the treatment of intermediate and advanced liver cancer, domestic scholars have done a lot of research. In 27 cases of PHC patients treated with body gamma knife, the tumor local control rate (CR+PR) was 81.5% three months after treatment. Kang Jingbo et al. applied body gamma knife to treat 152 patients with PHC, and the recent efficacy was 80.9%, and the 1-year survival rate was 41.5%. In this study, body gamma knife was applied to 52 patients with PHC, and the overall effective rate (CR+PR) was observed to be 76.92%, and the one-year survival rate was 67.65%. In this study, Kaplan-Meier analysis and Log rank test were performed on 52 patients with hepatocellular carcinoma with respect to gender, age, tumor T stage, presence of HBV infection, PVTT, Child-Pugh classification and whether to combine TACE treatment, and the results showed that the effect of Child-Pugh classification on prognosis was statistically significant (p=0.008). When gamma knife treatment is performed on PHC patients, the treatment side effects are not significant, and some patients may experience varying degrees of fatigue, nausea, vomiting, decreased white blood cells and platelets, fever and mild pain in the liver area, etc. The symptoms can generally be relieved after symptomatic treatment, and there is no need to interrupt the treatment. At present, many patients with liver cancer are already in the middle and late stages when they are diagnosed. The purpose of non-surgical treatment or comprehensive treatment such as radiation therapy and TACE is to resect the second stage and prolong survival with tumor. Body Gamma Knife treatment is suitable for some patients with intermediate and advanced liver cancer who refuse or are not suitable for surgery, and the vast majority of patients who receive Body Gamma Knife treatment can tolerate it. Thus, body gamma knife provides an effective treatment for patients with primary liver cancer who do not have indications for surgery or intervention or who are afraid of these treatments.