Cerebral malaria (CM) accounts for nearly 400,000 deaths annually inAfrican children. Current dogma suggests that CM results from infected RBC (iRBC)sequestration in the brain microvasculature and resulting sequelae. Therapies targetingthese events have been unsuccessful; findings in experimental models suggest that CD8+ Tcells drive disease pathogenesis. However, these data have largely been ignored becausecorroborating evidence in humans is lacking. This work fills a critical gap in ourunderstanding of CM pathogenesis that is impeding development of therapeutics.