Therefore, in future studies, it will be important to assess the influence of PRL on the GCs, as well as the interaction of B cells and TFH in an environment featuring high levels of PRL, to better understand the role of PRL in GC formation and to define the most important steps in the pathogenesis of SLE that could be targeted by antagonistic molecules (Figure 6). The gene discussed is PRL; the disease is systemic lupus erythematosus.