Canola (Brassica napus L.) has become a major field crop in Canada. One of the largest threats to canola production is the disease of clubroot caused by the soilborne pathogen Plasmodiophora brassicae. This disease can have devastating effects on canola yield and quality. Long-lived resting spores make this disease difficult to manage with few strategies proving to be effective. Currently, the most effective management tool is the development and deployment of host plant genetic resistance. We studied a double haploid population developed from crossing a male parent containing clubroot resistance genes PH1 and PH2 to a female parent containing clubroot resistance gene PH3. Molecular profiles for each of the three genes in the DH lines was determined. Planned crosses among a subset of the DH lines were then made to obtain 108 F1s with all possible homozygous and heterozygous combinations of PH1, PH2, and PH3.These 108 F1s 27 genotypes were tested in a greenhouse setting against P. brassicae pathotypes 3H, 3A, and 5X to phenotype their clubroot reaction. Disease index was compared between the 27 combinations of PH1, PH2, and PH3 represented within the 108 F1s. Results found evidence of an epistatic effect between PH2 and PH3 that improved disease resistance to a greater extent than was observed when either gene was in single heterozygous form. The results highlight the importance of verifying gene reactions through gene stacking to identify epistatic effects. Utilizing gene stacking could produce more durable and broad-spectrum clubroot resistant canola varieties.