Although the positive CSF GFAP–IgG on the 5th day after admission had suggested the possibility of GFAP-A, the significantly decreased CSF chloride (114.1 mmol/L) in the patient was consistent with the CSF characteristics of tuberculous meningitis.[4] Given that concurrent infection may exacerbate GFAP-A-related inflammation and interfere with treatment response, we initiated antituberculosis treatment alongside GFAP-A-targeted therapy to rule out the superimposed effect of tuberculosis on the patient’s condition. The gene discussed is GFAP; the disease is tuberculosis.