Although it is difficult to determine how the disease progressed in this patient, two interpretations are possible. Firstly, the patient could have developed lymphoproliferative lesions like LYG, which were progressive. Dormant EBV in B-cells could have become active due to immunosuppression by low-dose methotrexate and/or the immunosenescence of the host, and the cell-mediated immune response could have been provoked by humoral factors from the EBV-positive-B-cells and/or products of EBV. The exaggerated neuroinflammatory response, not the clonal expansion of the neoplastic cells, was the primary pathology of the disease. However, pathological evidence of EBV infection in this patient was weak; EBER expression was absent in the parotid gland, liver, and brain specimens. Moreover, expression of EBER was not ubiquitous in the atypical B-cells observed in the cervical lymph node.