Individuals with deficiencies in terminal complement components and in patients treated with the C5-specific inhibitor such as eculizumab carry increased susceptibility to invasive meningococcal infections (28) Increased susceptibility to Hib infection has been observed in individuals in particular with early complement component (C1, C2, C3, C4) deficiencies, but not C5 deficiency (19, 44–46) indicating that host defense against invasive Hib infection does not entirely rely on the lytic activity of the MAC of complement. The gene discussed is C4A; the disease is meningococcal infection.