Furthermore, FS patients with active disease present enhanced expression of the C1QA gene (an initiator molecule of the classical pathway) and increased serum levels of C3 and C-reactive protein (opsonins), of the cleaved factors resulting from the activation of the alternative pathway (Ba factor), or of the classical/lectin complement pathways (C4d factor), as well as a trend to decreased mannose-binding lectin serine protease 2 levels, reflecting activation of the lectin pathway (14, 22–24). This evidence concerns the gene C3 and Feingold syndrome.