Prolactin (PRL) is a versatile pleiotropic hormone produced by the anterior pituitary and multiple extrapituitary sites including immune cells 1. While recognized primarily for initiating lactation in females 2, PRL functions as both a hormone and cytokine with widespread physiological effects. PRL signals through prolactin receptors (PRL-R) distributed throughout the immune system via JAK-STAT pathway activation 1, particularly involving JAK2, Stat1, and Stat5 1. Beyond reproduction, PRL modulates immune function by stimulating B and T lymphocyte proliferation 3 and regulating cutaneous functions including keratin expression and hair growth 4. Clinically, elevated PRL levels are implicated in autoimmune diseases, particularly systemic lupus erythematosus (SLE), where mild-to-moderate hyperprolactinemia occurs in 20-30% of patients and correlates with active disease and lupus nephritis 1. PRL also functions as a risk factor for breast and prostate cancer 5. The hormone's autocrine and paracrine activities from locally produced PRL in target tissues suggest potential roles in pathophysiology, making PRL receptor antagonists promising therapeutic targets for conditions where local PRL may promote disease 6. Dopamine agonists that suppress PRL have demonstrated efficacy in treating autoimmune disorders 3.