Cryptosporidium parvum is a well-recognized cause of diarrhea in humans and animals throughout the world, and is associated with a substantial degree of morbidity and mortality in patients with acquired immunodeficiency syndrome (AIDS). Despite intensive efforts over the past 20 years, there is currently no effective therapy for treating or preventing infection by C. parvum. Until recently, the development of effective anticryptosporidial therapies has been hindered by the paucity of biological targets for structure-based drug design. With the pending completion of sequencing of the entire C. parvum genome, there should be no lack of potential biological targets for development of specific inhibitors. What are needed are focused efforts to identify essential parasite biochemical pathways for which specific inhibitors can be developed that are safe to the host. Analysis of the currently available sequences has identified specific aspects of C. parvum biochemistry that are unique relative to mammals. In addition, the ongoing genome efforts are providing a clearer picture of the biology of the apicomplexan parasites. It is becoming evident that C. parvum uses distinct approaches to solve basic metabolic needs as compared to Plasmodium falciparum and Toxoplasma gondii. These differences suggest that therapies developed for these model apicomplexans may not necessarily be effective against cryptosporidiosis, and emphasizes the importance of understanding the unique biology of C. parvum.