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Host/pathogen studies often focus on large effect genes in epidemic pathogens. This has developed a general molecular model where the interaction of proteins or metabolites from the host and pathogen trigger an “immune” response to create qualitative resistance. It is not clear how this model translates to broad host range endemic quantitative pathogens. To test this, we sequenced the genome of 96 diverse Botrytis cinerea isolates. The pathogen contains high levels of genetic with evidence for diversifying selection at known virulence loci such as toxin metabolite clusters and cell wall degrading genes. However, most selected regions had loci previously not linked to virulence and are likely identifying new virulence mechanisms. We used this genetic variation in the pathogen to study the host by infecting all 96 isolates on Arabidopsis thaliana and measuring both species transcriptomes. This identified extensive interaction between the two species centering on pathogen toxin production and host photosynthesis. Genome wide association mapping of virulence and the two transcriptomes showed a highly polygenic architecture controlling the interaction. This included hotspots in the pathogens genome that controlled virulence as well as a large number of transcripts in either the host or pathogen. We are extending this analysis to other dicots including Tomato, Lettuce, Chicory, Sunflower, Soybean and Brassica. Virulence on these species highly polygenic with a minimal effect of domestication on the host/pathogen interaction. Most plant species showed an increased resistance in the domesticated germplasm and a similar range of variation between wild and domestic germplasm.