Additionally, Peli1 is dispensable for BCR-mediated B cell activation, suggesting increased production of autoantibodies and B cell activation during SLE pathogenesis in Peli1-deficient mice is attributing to the promoted activation of noncanonical NF-κB pathway but not from TLR or BCR signaling. Here, NFKB1 is linked to systemic lupus erythematosus.