We hypothesized that PRL-LFPRLR signaling may induce AID expression because (1) estradiol, which promotes Aicda transcription and accelerates malignant transformation of B-lymphocytes in MRL-lpr mice51 could, in part, mediate this process via stimulation of PRL secretion, and (2) a reduction in both DCs that mediate CSR, and LLPC that result from class-switched B cells in LFPRLR SMO-treated SLE-prone mice suggested that PRL-LFPRLR signaling may regulate AID expression. The gene discussed is PRL; the disease is systemic lupus erythematosus.