However, in those diseases mediated by thrombin that have a C3-independent C5 activation, such as acute lung injury (Huber-Lang et al., 2006), LPS-induced fetal loss (Yu et al., 2008), and autoantibody-meditated arthritis (Auger et al., 2012), C3−/− mice still had the same disease susceptibility as wild-type mice. The gene discussed is C3; the disease is Arthritis.