The New Zealand wheat (Triticum aestivum L.) cv. Karamu (same parentage as the US cv. Anza) was originally believed to carry gene Yr18, which provides adult plant resistance to stripe rust (Puccinia striiformis f. sp. tritici), in addition to the seedling resistance gene YrA. Following the detection of virulence to the stripe rust resistance gene YrA in 1995, much of the resistance of Karamu was eroded and the cultivar suffered from occasional severe stripe rust outbreaks. This meant that either one or more new races of Puccinia striiformis f. sp. tritici with virulence to Yr18 had developed, or that Yr18 conferred inadequate resistance under high disease pressure. Karamu was crossed with cv. Otane, which carries Yr18, and 140 double haploid (DH) lines obtained from the F₁ progeny were evaluated for seedling and adult plant resistance under greenhouse and field conditions. Evaluation of F₁ plants against stripe rust pathotype 106E139A⁺ revealed that the resistance was recessive and that none of the resistance genes present was effective at the seedling stage. Segregation in the DH lines at the adult plant stage indicated that the resistance measured through infection type in both the greenhouse and the field was based on 3 genes, 1 from Karamu and 2 from Otane. However, the resistance gene from Karamu did not contribute towards resistance measured through final disease severity, but acted additively with genes from Otane in providing slow-rusting resistance as expressed by lower values for area under the disease progress curve. It was concluded that Karamu does not have gene Yr18, but rather possesses a recessive minor gene, which explains its adult plant susceptibility under high disease pressure. However, this Karamu gene did interact with Otane resistance genes to provide increased resistance.