D2R agonist, such as bromocriptine, suppresses PRL secretion to decrease HPRL and to normalize the dopaminergic system in SLE, through the pertussis toxin (PTX)-sensitive Gi/o and PTX-insensitive Gz proteins, as well as a G protein-independent, β-arrestin/glycogen synthase kinase-3-dependent pathway (150, 151). This evidence concerns the gene DRD2 and systemic lupus erythematosus.