It has been suggested that one of the main factors which determines host susceptibility to different malarial parasites is the interaction of their invasive forms, merozoites, with specific receptors on the red cell membrane1–3. Thus the Duffy blood group determinants may be involved in the entry of Plasmodium vivax but not of Plasmodium falciparum into human red cells. When analysing red cells deficient in various blood group antigens, Miller et al. noted3 that two samples of En(a−) cells showed a reduction of invasion by P. falciparum4. These cells lack both the major transmembrane sialoglycoprotein, glycophorin A (or MN glycoprotein), and the independently segregating Wrightb (Wrb) antigen and also show increased glycosylation of band 3, the major membrane-penetrating glycoprotein. Despite this, En(a−) individuals are haematologically normal5. We have now confirmed that En(a−) cells obtained fresh from three En(a−) individuals are indeed relatively resistant to invasion by P. falciparum although they are able to support parasite development. Our results also indicate that these cells may be a useful model in the search for a putative receptor for P. falciparum.