Thus, clinical protocols have been developed in which clinical researchers should use D2R agonists, such as bromocriptine and cabergoline, to lower prolactin synthesis and secretion by infiltrating synovial fibroblasts and lymphocytes in patients with RA—the improvement in RA activity might be attributed to a significant decrease in the secretion of prolactin by immune cells [247, 248], although these results are not conclusive. Here, PRL is linked to rheumatoid arthritis.