For example, B-cell-conditional ablation of Peli1, an E3 ubiquitin ligase that mediates ubiquitin-dependent NIK degradation in B cells, induces autoantibody production in lupus-like disease via noncanonical NF-κB activation, whereas overexpression of Peli1 inhibits noncanonical NF-κB activation and alleviates lupus-like autoimmune symptoms [225]. The gene discussed is NFKB1; the disease is systemic lupus erythematosus.