Toxoplasma gondii infection is acquired by oral ingestion. After dissemination, tachyzoites differentiate into bradyzoites within cysts that remain latent. The ability of bradyzoites to transform back into tachyzoites is a central factor in the ability of T. gondii to reactivate and cause disease in immunosuppressed individuals. Both tachyzoites and bradyzoites develop in tissue culture. Recent advances in the genetic manipulation of T. gondii have expanded the molecular tools that can be applied to studies on bradyzoite differentiation. Evidence is accumulating that this differentiation event is stress mediated and may share common pathways with stress-induced differentiation events in other eukaryotic organisms. Bradyzoite differentiation defective mutants have been studied using microarray analysis, allowing identification of genes that may be coordinately regulated during this stage transition. Characterization of unique bradyzoite-specific structures, such as the cyst wall, and stage-specific metabolic pathways are other approaches being used to study developmental stage conversion.