Preclinical and clinical evidence supports this mechanism (23, 24): anti-CTLA-4 monoclonal antibody induces pituitary inflammation through complement-mediated cytotoxicity in a mouse model; autopsy studies have shown strong CTLA-4 expression in the pituitary gland of the patients as well as pathological features consistent with both type II (antibody-mediated) and type IV (T-cell-mediated) hypersensitivity; and antipituitary hormone antibodies (e.g., anti-ACTH antibodies) are detected in the patient serum. Here, CTLA4 is linked to inflammatory response.