This results in the three main mechanisms by which complement directly prevents infection: (1) opsonisation and increased phagocytosis of the pathogen by covalent linkage of C3b and iC3b to bacterial surface molecules; (2) pro-inflammatory signaling by the complement components C3a and C5a; and (3) direct killing of the pathogen by formation of the membrane attack complex, a lipophilic complex of the terminal complement components which forms a pore in the pathogen phospholipid bilayer leading to bacterial lysis (Walport, 2001). The gene discussed is C3; the disease is infection.