Host-selective toxins are known determinants of compatibility in plant–fungus interactions and provide a powerful model for understanding the specificity of these associations. The identification of genes required for toxin biosynthesis has shown that the genes are unique to the toxin producing species and are clustered in complex loci. These loci may have been acquired by horizontal gene transfer. Many, if not all, host-selective toxins act by disrupting biochemical processes and in several cases the resulting cell death has the characteristics of programmed cell death. This ability to make dead tissue from living has enabled these facultative saprophytic fungi to become plant pathogens.