Apicomplexan parasites cause diseases of medical and agricultural importance linked to dramatic changes they impart upon infected host cells. Following invasion, the malaria parasite Plasmodium falciparum renovates the host erythrocyte using mechanisms previously believed to be malaria-specific. This involves proteolytic cleavage of effectors in the endoplasmic reticulum that licences proteins for translocation into the host cell. Recently, it was demonstrated that the related parasite Toxoplasma gondii, responsible for disease in immunocompromised individuals and congenital birth defects, has an analogous pathway with some differences, including proteolytic processing in the Golgi. Here we review the similarities and distinctions in export mechanisms between these and other Apicomplexan parasites to reconcile how this group of pathogens modify their host cells to survive and proliferate.