Although the B-cell repertoire was normally distributed after LFPRLR knockdown, frequencies of potentially abnormal B cells with long CDR3s ranging from 35-42 amino acids, and those with non-functional IGH rearrangements were significantly reduced in LFPRLR SMO-treated SLE-prone mice (Fig. 2e–g). The gene discussed is SMO; the disease is systemic lupus erythematosus.