One of the most successful protozoans is the malaria parasite, which has evolved key mechanisms to avoid the host immune system. This theme was recently reviewed with a focus on their capacity to overcome both innate responses, and the induction and maintenance of adaptive immune responses (Gomes, Bhardwaj et al.; Rénia and Goh; Gomes, Feijó et al.). With regards to this topic, the authors highlighted the importance of carbohydrate-mediated interactions that directly affect Plasmodium survival and host resistance. Plasmodium parasites have a complex life cycle in the vertebrate host. Initial stages comprise infection of hepatocytes, in which the CSP and TRAP domains of the sporozoite form of the parasite mediate an adhesive interaction with sulfated glycoconjugates on the surface of hepatocytes, initiating the intracellular parasitism stage in the host. The dependency on carbohydrate-mediated interactions for the parasitism also continues in the bloodstream form of the parasite via carbohydrates expressed by red blood cells, such as ABO, Lewis, and Duffy, which thereby influences erythrocyte parasitism.