Widespread endothelial activation (including increased ICAM-1 expression and the disruption of cell-junction proteins) has been observed in postmortem studies of cerebral malaria patients [36], and markers of endothelial activation and dysfunction such as soluble ICAM-1, von Willebrand factor, and angiopoietin-2 are elevated in cerebral malaria [37–39]. This evidence concerns the gene ANGPT2 and cerebral malaria.