The etiology of lymphoma is of great concern to most lymphoma patients and their families. In fact, the etiology and pathogenesis of lymphoma are not fully understood so far, and scholars at home and abroad mainly focus on several factors such as virology, Helicobacter pylori, and abnormal immune function. In patients with Burkitt’s lymphoma, more than 80% of patients have significantly higher titers of EBV antibodies in their sera, while only 14% of non-Burkitt’s lymphoma patients have higher titers. Those with high titers also had a significantly higher chance of developing Burkitt’s lymphoma. EBV may also be the cause of post-transplant lymphoma and AIDS-associated lymphoma. Retroviruses were proposed to be closely related to the development of lymphoma in the late 1970s. In Japan, a clear trend of family concentration and regional prevalence of adult T-cell lymphoma/leukemia was found. Human T-cell leukemia/lymphoma virus (HTLV1) was shown to be the cause of this type of T-cell lymphoma (see Leukemia). Another retrovirus, HTLV II, has recently been implicated in the development of T-cell cutaneous lymphoma (mycosis fungoides). kaposi sarcoma virus has also been implicated as the cause of primary body cavity lymphoma (PBCL). Gastric mucosal hypolymphoma is a B-cell mucosa-associated lymphoid tissue lymphoma, and the presence of H. pylori is closely associated with its development, and H. pylori is now considered to be the etiology of this lymphoma. The immune function of the patient is also associated with the development of lymphoma. In recent years, it has been found that more patients with hereditary or acquired immunodeficiency have lymphoma than normal people; 1/3 of the patients who develop malignant tumors after long-term application of immunosuppressants after organ transplantation are lymphoma. The number of lymphomas in patients with dry syndrome is higher than that of the general population.