The finding that the prolactinoma-associated Asn492Ile PRLR variant resulted in a gain of function that increased pAkt signaling, which is known to have a role in the etiology of other neoplasms (e.g. carcinomas of the breast, ovary, colon, pancreas and liver, non-Hodgkin’s lymphoma and pituitary tumors; 2,32–37), and proliferation indicated that it may have a role in the development of prolactinomas via prolactin-induced Akt activation. This evidence concerns the gene PRL and non-Hodgkin lymphoma.