Foxp3 was originally suspected to be important for Treg functions because mutations in Foxp3 were found to be the cause of two severe multiorgan autoimmune syndromes in humans, namely XLAAD (X-linked autoimmunity-allergic dysregulation syndrome) and IPEX (immunodysregulation, polyendocrinopathy, enteropathy, X-linked syndrome) [122–124]. Here, FOXP3 is linked to polyendocrinopathy.