Recent work studying the host genetic contribution to severe malaria identified a SNV allele at a nearby non-repeated region in linkage disequilibrium with a complex structural variant at the glycophorin locus protective against severe malaria.5, 20 This structural variant, called DUP4, is restricted to East African populations and is responsible for a glycophorin B-glycophorin A fusion gene product that is detected using serology as the blood group antigen Dantu NE+. This DUP4 variant confers a clinically important protective effect, with carriers ∼40% less likely to develop cerebral malaria.5 Given that glycophorin A and glycophorin B are erythrocyte receptors for the Plasmodium falciparum cell surface receptors MSP-1, EBA-175, and EBL-1, respectively, it is likely that this protective effect is mediated by an altered ability of the parasite to invade the host erythrocyte.25, 26, 27, 28