With a decrease in susceptibility by an estimated factor of 5 to 10 (based on survival rates in C5ar1−/− or C5aR1 antagonist-treated mice), the impact on IMD of C5a-derived inflammation has a smaller amplitude than but a direction clearly opposite from that of opsonization (C3−/−) and bacteriolysis (Hc°/°) in our N. meningitidis sepsis model. The gene discussed is C5; the disease is Sepsis.