Postmortem samples from children who died from cerebral malaria show activation of endothelial cells (with upregulation of ICAM-1) and macrophages (with increased macrophage scavenger receptor and sialoadhesin), and disruption of endothelial intercellular junctions (ZO-1, occludin, vinculin) in vessels containing sequestered parasitized red blood cells. The gene discussed is ICAM1; the disease is cerebral malaria.