Our studies have highlighted that a gain of functional activity within the pAkt pathway may be an important mechanism in pituitary tumorigenesis in patients with the Asn492Ile PRLR, and this may be analogous to the increased pAkt signaling that has been reported to have an etiological role in other neoplasms (e.g. in carcinomas of the breast, ovary, colon, pancreas and liver, non-Hodgkins Lymphoma and pituitary tumors; (2,32–37)). The gene discussed is PRLR; the disease is non-Hodgkin lymphoma.