Malaria parasites operate antigenicvariation systems to avoid antibody recog-nition, thereby inhibiting their host’scapacity to clear infections [1]. Plasmodi-um falciparum, the most pathogenic of thehuman malaria species, bases immuneevasion on switching expression of ap-proximately 60 var genes. These encodetransmembrane proteins (PfEMP1 anti-gens) on the red blood cell surface, whichallow intraerythrocytic (IE) parasites toadhere to endothelial molecules [2].PfEMP1 proteins are thus not simplyantigenic decoys, but functional vascularadhesion receptors. The disappearance ofolder parasites from the bloodstreamresults from PfEMP1 binding to endothe-lial receptors, a process called sequestra-tion. This enables replicating stages toavoid the dangerous passage through thespleen, the main organ of defence againstblood infection [3]. In this issue, Claessenset al. [4] present new and intriguing dataon how antigenic diversity can be contin-uously generated during persistent malariainfections.