Tan spot, caused by the fungus Pyrenophora tritici-repentis, is an important foliar disease of wheat. Eight races of P. tritici-repentis have been identified to date, based on their ability to cause necrosis and/or chlorosis on a set of wheat differential hosts. These symptoms result from the action of host-specific toxins, which are produced in different combinations by races of the fungus and mediate the interaction between host and pathogen. Ptr ToxA induces necrosis on sensitive wheat genotypes, and is a 13.2 kDa protein encoded by the ToxA gene. Ptr ToxB, encoded by the ToxB gene, is a 6.6 kDa, chlorosis-inducing protein. Ptr ToxC also induces chlorosis, but appears to be a non-proteinaceous, polar, non-ionic, low-molecular-mass molecule. In susceptible wheat, three dominant and independently inherited toxin-sensitivity genes have been identified, each controlling the reaction to a single toxin. Most studies have also found that sensitivity to the toxins and susceptibility to the producing races co-segregate, and appear to be controlled by the same genes. Therefore, the tan spot pathosystem conforms to the toxin model of host-pathogen interactions, in which the compatible interaction is the basis for specificity (as opposed to the incompatible interaction in the classical gene-for-gene model). It is likely that P. tritici-repentis produces additional toxins or pathogenicity factors, but these remain to be identified.