Another reason for irAE development could be the differential expression of these molecules on the body’s normal tissues, as exemplified by CTLA-4 expression in hypophyseal cells, which can lead to anti-CTLA4 related hypophysitis, as well as PD-L1 expression on pancreatic islet cells, which can induce type I diabetes upon PD-L1 targeting [69]. Here, CTLA4 is linked to hypophysitis.