Therefore, different levels of expression of the PRL receptor at the protein level and a discordant network of the regulation of genes related to apoptosis may explain, on one hand, why we did not observe STAT3 phosphorylation and rescue of apoptosis in C57BL/6 immature B cells, and, on the other hand, the capacity of PRL to trigger SLE specifically in individuals with genetic susceptibility. The gene discussed is PRL; the disease is systemic lupus erythematosus.