Many bacterial diseases of plants depend on the interaction of type III effector genes of the pathogen and disease-susceptibility genes of the host. The host susceptibility genes are largely unknown. Here, we show that expression of the rice gene Os8N3, a member of the MtN3 gene family from plants and animals, is elevated upon infection by Xanthomonas oryzae pv. oryzae strain PXO99 A and depends on the type III effector gene pthXo1. Os8N3 resides near xa13, and PXO99 A failed to induce Os8N3 in rice lines with xa13. Silencing of Os8N3 by inhibitory RNA produced plants that were resistant to infection by strain PXO99 A yet remained susceptible to other strains of the pathogen. The effector gene avrXa7 from strain PXO86 enabled PXO99 A compatibility on either xa13-or Os8N3-silenced plants. The findings indicate that Os8N3 is a host susceptibility gene for bacterial blight targeted by the type III effector PthXo1. The results support the hypothesis that X. oryzae pv. oryzae commandeers the regulation of otherwise developmentally regulated host genes to induce a state of disease susceptibility. Furthermore, the results support a model in which the pathogen induces disease susceptibility in a gene-for-gene manner.A virulence genes and their cognate host R genes, contribute to the basis of the so-called gene-for-gene model of hostpathogen incompatibility, and many avirulence and R gene pairs have been characterized, along with attempts to explain the associated signaling pathways for resistance (1). The outcome of host-pathogen interactions is also controlled by compatibility factors, which consist of virulence factors in the pathogen and susceptibility factors of the host. In plant pathogenic bacteria, important contributions to compatibility are provided by the type III secretion system (TTSS), which functions in the secretion and injection of substrate proteins (type III effectors) into eukaryotic host cells (2, 3). Type III effectors of plant pathogens presumably function similarly to effectors of animal pathogens and target various host-susceptibility factors (4, 5). In contrast to the effectors of the animal pathogens and R genes of plants, however, few host-susceptibility targets of type III effectors from plant bacterial pathogens have been identified.