In humans, there is evidence that increased levels of a secreted form of P-selectin are found in patients presenting with non-severe versus severe malaria [5], possibly by out-competing and reducing interactions between membrane-tethered endothelial P-selectin and the parasite ligand PfEMP1, which is displayed on the surface of infected erythrocytes [8, 13]. The gene discussed is SELP; the disease is malaria.