Germline genetic abnormalities associated with pituitary tumor pathogenesis include inactivating mutations of menin in patients with Multiple Endocrine Neoplasia type 1 [6]–[7], loss of function mutations of the aryl hydrocarbon receptor-interacting protein (AIP) tumor suppressor gene in patients with familial isolated pituitary adenomas [8], and activating mutations the Protein kinase A type I regulatory subunit PRKA [9] in patients with Carney complex, however these alterations have not been shown to mediate pituitary neoplastic growth in the more common sporadic neoplasms. The gene discussed is AIP; the disease is multiple endocrine neoplasia type 1.