Thus, lack of autocrine CD46 activation, such as in CD46- and C3-deficient patients, results in subnormal Th1 cell responses (Le Friec et al., 2012), whereas uncontrolled autocrine C3 activation and dysregulated CD46 engagement contribute to hyperactive Th1 cell responses in autoimmune pathologies (Astier et al., 2006; Cardone et al., 2010; Liszewski et al., 2013). The gene discussed is C3; the disease is Autoimmunity.