At this stage, mechanisms which augmented the pathogenicity of B cell repertoire in SLE and LN include enhanced RAG expression and BCR signaling, increased somatic hypermutation (SHM) and class-switch recombination (CSR), aberrations in B cell transcription factors (e.g., BACH2, BLIMP1) and increased expression of B cell-related cytokines (e.g., BAFF, IL-6 and IL-21). This evidence concerns the gene PRDM1 and systemic lupus erythematosus.