CP activation is assumed to play a role in initial pathogenic complement activation in lupus nephritis since both lupus patients and lupus-prone mice exhibit significant glomerular IC deposition consisting of auto-Ag–auto-Ab complexes (e.g., dsDNA-anti-dsDNA Ab complexes) and C1q, a recognition molecule for the CP. Here, RENBP is linked to systemic lupus erythematosus.