The necrotrophic fungal pathogen Stagonospora nodorum produces multiple necrotrophic effectors (NEs), also known as host-selective toxins, which interact with corresponding wheat genes in an inverse gene-for-gene manner to cause the disease Stagonospora nodorum blotch (SNB). In previous research, we showed that the homoeologous wheat genes Snn3-B1 and Snn3-D1, located on wheat chromosome arms 5BS and 5DS, respectively, both recognize the NE SnTox3 to confer effector-triggered susceptibility. Here, we describe genome analysis and mapping results from ongoing efforts to clone the two Snn3 genes. Saturation mapping of the genes in relatively small F2 populations using SSRs and EST-derived markers followed by comparative analysis with the rice and Brachypodium genomes revealed that both the Snn3-B1 and Snn3-D1 regions were highly conserved with regions of rice chromosome 12 and Brachypodium chromosome 4. This colinearity allowed us to develop numerous additional markers to further saturate the Snn3-B1 and -D1 regions. Subsequent fine-mapping of both genes in large F2 populations resolved some co-segregating markers and delineated the genes to small intervals. BAC contigs identified with flanking markers were anchored to the Snn3-D1 genetic map. The ratio of physical to genetic distance in the Snn3-D1 region was estimated to be 500-800 kb/cM. Because these two NE sensitivity genes are homoeologous, we can work towards cloning them in parallel, and once cloned, we can study their evolutionary history and investigate their functional roles in mediating recognition of SnTox3.