Plasmodium falciparum causes cerebral malaria in humans, and nearly all malaria deaths result from infection by this species. Observations suggest that heat shock proteins play a key role in the management of toxicity conferred by drugs to the parasite, and may augment drug resistance. In addition to their role within the parasite, growing evidence suggests that parasite heat shock proteins are involved in the trafficking of parasite-encoded proteins to the erythrocyte surface, thus playing a key role in the pathogenesis of P. falciparum malaria.