The role of bromocriptine as primary therapy for prolactin-producing tumors is currently well accepted in the literature. Bromocriptine decreases the concentration of serum prolactin and this decrease precludes tumor shrinkage, despite the lack of correlation between amount of decrease in tumor size and baseline serum prolactin. We submit the case of a patient on chronic bromocriptine therapy followed by measuring baseline and thyrotropin-releasing hormone (TRH)-stimulated serum prolactins. Bromocriptine affects both release and storage of prolactin. The literature has suggested that the effects of bromocriptine on storage and synthesis may be responsible for its effects on tumor size. It was felt that TRH stimulation would more accurately reflect storage and synthesis, and thus correlate better with tumor size. The pituitary was initially debulked via a right frontal approach; then the patient was placed on bromocriptine therapy and postoperatively followed with baseline and TRH-stimulated serum prolactins. The size of the pituitary was measured by computed tomography. Baseline serum prolactin levels rapidly decreased, but despite the slow decrease in TRH-stimulated prolactins no change was noted in tumor size. Because of the time difference between the baseline and TRH-stimulated prolactin levels, we conclude that clinically bromocriptine affects primarily secretion of prolactin and secondarily storage and synthesis. We also show that TRH-stimulated prolactin does not correlate with size of prolactin-secreting pituitary tumors and therefore tumor size should be independently measured. The literature has shown that prolactinomas do not respond well to TRH stimulation. Because bromocriptine in our patient affects secretion of prolactin prior to synthesis and storage, we believe that bromocriptine makes it appear that TRH stimulation is enhancing prolactin response and not that the effect of bromocriptine has enhanced sensitivity of the tumor to TRH.