Germline genetic abnormalities associated with pituitary tumor pathogenesis include inactivating mutations of menin in patients with Multiple Endocrine Neoplasia type 1 [5, 6], loss-of-function mutations of the aryl hydrocarbon receptor-interacting protein (AIP) tumor suppressor gene in patients with familial isolated pituitary adenomas [7], and inactivating mutations the Protein kinase A type I regulatory subunit PRKAR1A [8] in patients with Carney complex, however these alterations have not been shown to mediate pituitary neoplastic growth in the more common sporadic neoplasms. Here, AIP is linked to pituitary gland adenoma.