An autopsy of patients who died after IH revealed that their pituitary tissue expressed CTLA-4, especially on pituitary TSH and PRL cells [42,43], suggesting that CTLA-4 inhibitors can directly bind to CTLA-4 on pituitary cells and degrade it as an antigen presented to CD8+ T cells, eventually inducing IH through the type IV hypersensitivity system [44]. Here, CTLA4 is linked to isolated hemihyperplasia.