Recently, Sato et al. reported that lupus patients with MBL/L-ficolin and properdin deposition in their glomeruli had significantly higher urinary protein excretion levels compared to patients without glomerular deposition, suggesting pathogenic and exacerbating roles for the LP and AP in the development of lupus glomerulonephritis (27). The gene discussed is CFP; the disease is systemic lupus erythematosus.