This chapter reviews the genetics, pathology, and molecular biology of T-cytoplasm male sterility in maize. The chapter discusses the role of cytoplasmic male sterility systems in facilitating the production of hybrid seeds. The effects of widespread planting of T-cytoplasm maize on the severe 1970 epidemic and effect of a mitochondria1 gene on disease susceptibility and male sterility are discussed. It also discusses the involvement of nuclear cytoplasmic interactions in restoration of cms-T, the perspectives of cms-T researchers, and future directions. In cms-T plants, male sterility is associated with premature breakdown of the mitochondria-rich, tapetal cell layer of the anther; this layer is crucial to pollen production because it supplies nutrients to the developing microspores. In many species, cms is associated with the expression of novel open-reading frames in the mitochondrial genome. The studies provided a foundation for further research that resulted in the cloning of the T-urf13 and Rf2 genes from maize and the ChPKSl gene from C. heterostrophus, and the generation of models for the topology of urf13 in the inner mitochondrial membrane, Rfl-mediated processing of T-urfl3 transcripts, and the evolution of toxin biosynthesis in C. heterostrophus and M. zeae-maydis.