In dopamine-resistant prolactinomas, the increased expression of somatostatin receptors (especially SSTR5 and SSTR1) leads to inhibited prolactin secretion by reducing cAMP levels, allowing for targeted therapies like octreotide and pasireotide, which can variably affect tumor size and PRL levels, while peptide receptor radionuclide therapy has shown potential but requires careful patient selection for effectiveness [1, 13–17]. This evidence concerns the gene PRL and prolactin-producing pituitary gland adenoma.