Studies on first-generation somatostatin analogues (SSAs) have shown no efficacy in the treatment of resistant prolactinomas as they bind primarily to somatostatin receptor subtype 2a (SST2a), while somatostatin receptor subtype 5 (SST5) is more important in PRL secretion [1,5]. This evidence concerns the gene SSTR5 and prolactin-producing pituitary gland adenoma.