The identity of cell surface receptor molecules on Plasmodium falciparum-infected erythrocytes is of great interest since the functional sites involved in attachment to endothelial cells may be structurally conserved in wild isolates. Such conserved sites may represent suitable antigenic targets for a vaccine-induced immune response that would block or reverse infected cell sequestration in vivo. Identification of the infected cell receptor sites may also lead to novel methods for treatment of acute cerebral malaria. We review the likely roles, either direct or indirect, for the participation of knob protrusions, malarial proteins expressed at the cell surface, and modified host membrane proteins in the specific receptor properties acquired by infected erythrocytes.