Because addition of P. falciparum-infected plasma to EC [107] or cytoadherance is associated with TF expression [10], ROS production [105], apoptosis [108], and activation of NF-κB [109], it is plausible that therapeutic targeting of O2− would be effective to prevent the endothelial activation observed in severe malaria [110]. The gene discussed is NFKB1; the disease is malaria.