The effect of the SnTox3-Snn3 interaction was documented for the first time under natural infection at the adult plant stage in the field. Co-segregating SNP markers were identified. Parastagonospora nodorum is a necrotrophic pathogen of wheat, causing Septoria nodorum blotch (SNB) affecting both the leaf and glume. P. nodorum is the major leaf blotch pathogen on spring wheat in Norway. Resistance to the disease is quantitative, but several host-specific interactions between necrotrophic effectors (NEs) and host sensitivity (Snn) genes have been identified, playing a major role at the seedling stage. However, the effect of these interactions in the field under natural infection has not been investigated. In the present study, we saturated the genetic map of the recombinant inbred (RI) population SHA3/CBRD × Naxos using the Illumina 90 K SNP chip. The population had previously been evaluated for segregation of SNB susceptibility in field trials. Here, we infiltrated the population with the purified NEs SnToxA, SnTox1 and SnTox3, and mapped the Snn3 locus on 5BS based on sensitivity segregation and SNP marker data. We also conducted inoculation and culture filtrate (CF) infiltration experiments on the population with four selected P. nodorum isolates from Norway and North America. Remapping of quantitative trait loci (QTL) for field resistance showed that the SnTox3-Snn3 interaction could explain 24% of the phenotypic variation in the field, and more than 51% of the variation in seedling inoculations. To our knowledge, this is the first time the effect of this interaction has been documented at the adult plant stage under natural infection in the field.