Several cytokines are known to take part in the endothelial dysfunction associated with leucocytes and infected red blood cells sequestration via the induction of intercellular-adhesion-molecule-1 (ICAM-1) and endothelial-protein-C-receptor (EPCR) expression on the cell surface and also by modulation of their shedding in the blood circulation resulting in an increased level of soluble EPCR and ICAM-1 (sEPCR, sICAM-1) in children admitted to the hospital for severe malaria [4,6,7,8]. The gene discussed is ICAM1; the disease is endothelial dysfunction.