Clinical symptoms of malaria are caused by a cascade of events triggered by the release of parasite "toxins" at the time of schizont rupture. The production of cytokines, particularly TNF alpha, plays a central role in this cascade. In addition to TNF, the pathogenesis of cerebral malaria (the most severe form of the disease) also requires the existence of cytoadherence of infected erythrocytes in cerebral capillaries and the intensity of this cytoadherence is controlled by a mixture of host and parasite features. Finally, anti-parasite and anti-toxic immunity (or "premunition") play a role in the reduction of pathology in individuals living in endemic areas.