(1) C5 deficient mice were resistant to cerebral malaria, whereas C5aR deficient and C3aR deficient mice were susceptible. (2) C9 deposition was detected throughout the cortex of infected mice. C9 deposits frequently colocalized with blood vessels, while some were detected in the parenchyma. (3) anti-C9 antibody treatment significantly delayed the progress of cerebral malaria. This evidence concerns the gene C5AR1 and cerebral malaria.