Peli1 has been demonstrated to be involved in the control of B cell autoantibody production in systemic lupus erythematosus via a negative regulator of the noncanonical NF-κB pathway in B cells resulting in the production of more antibodies, specifically promoting the IgG2a class-switch in Peli1-deficient mice [11]. This evidence concerns the gene NFKB1 and systemic lupus erythematosus.