It has been demonstrated that excessive GHRH stimulation leads to somatotroph hyperplasia and, ultimately, pituitary adenoma formation in metallothionein promoter-driven human GHRH transgenic mice (19), some of which had shown focal positivity for prolactin, further emphasizing the phenomenon of specificity spillover akin to thyro-lactotroph hyperplasia in long-standing untreated juvenile hypothyroidism (20). Here, PRL is linked to pituitary gland adenoma.