The evasion and subversion of immune responses during infection has elucidated many interesting and ingenious pathways used by pathogens to survive, expand, and eventually be transmitted to new hosts. These immune evasion mechanisms are of interest as they frequently suggest ways to prevent pathogens from causing infection or disease. More rarely, they make us consider or evaluate the whole strategy of vaccine or disease prevention. The Plasmodium species that cause malaria have classical immune evasion strategies through apparently immunologically distinct replication cycles and sites with the host and polymorphic and clonally variant antigens (1, 2). Recently, the human parasite Plasmodium falciparum was shown to modulate host defences more directly by altering the function of antigen-presenting cells (3, 4). The paper in this issue by Ocaña-Morgner et al. (5) describing inhibition of CD8+ T cell responses during murine malaria infection extends these observations and not only suggests a novel scheme of immune subversion by the parasite, but also poses important questions for the existing strategies to develop a vaccine against malaria.