The cloning of avirulence genes has greatly aided our understanding of plant-pathogen specificity. It has proven that the gene-for-gene relationship first noted by Flor is correct--single avirulence gene encoding single protein products indeed are the genetic elements that interact with plant disease resistance genes. Furthermore, firm genetic evidence has provided insight into how two cloned avirulence genes (the TMV coat gene and avrD) cause the HR. The differences in structure of pathogen elicitors also indicates that plants have evolved diverse recognitional mechanisms to detect pathogens. It is appealing to speculate, therefore, that elicitors represent the plant equivalent of antigens in vertebrates. Another consequence of these results has been the establishment of firm genetic and biochemical evidence supporting the elicitor-receptor model for recognition of incompatible pathogen races by plants. In both TMV and bacterial pathogens, we are also beginning to understand how avirulence genes are altered to confound plant recognition of the pathogen. The next few years should yield additional information on avirulence gene structure as well as the important questions of their function in the pathogen and the molecular mechanisms whereby plant recognition occurs. The marked successes in cloning avirulence genes underscore only more forcefully the pressing need to clone and characterize plant disease resistance genes. Certainly an understanding of these genes is required to further our basic knowledge of active defense in plants and to permit their manipulation for improved control of plant diseases in practical agriculture.