In tree-based intercropping, trees are established in rows, creating alleys that allow the mechanized production of crops. In 2004–2005, soybean (Glycine max) diseases were surveyed at the University of Guelph Agroforestry Research Station (established in 1987–1988, Guelph, Ont., Canada). This intercropping experiment is composed of 10 tree species, including black walnut (Juglans nigra). Areas within the soybean intercrop with symptoms of stunting, root rot, and interveinal chlorosis or necrosis were observed. In 2004 and 2005, these patches covered 253 and 738 m2, respectively, in the intercrop and were all found in the vicinity of black walnut. No patches were found in an adjacent soybean monoculture. Fusarium solani was isolated from diseased plants and Koch postulates completed, but the pathogen did not induce the stunting symptoms observed in the field. A role for juglone, an allelopathic compound produced by black walnut, as a predisposing factor to F. solani infection was investigated. The growth rate of F. solani at 1 × 10 4 mol/L juglone was reduced in vitro by 0.9 mm/day but not at a concentration of 0, 1 × 10−7, 1 × 10−6, and 1 × 10 −5 mol/L. In a hydroponic system, soybean was challenged with juglone (1 × 10−6 1 × 10−6, and 0 mol/L) and F. solani. Growth of soybean was severely reduced at 1 × 10−5 mol/L juglone, which can explain the observed stunting. Six days after infestation, plants challenged with juglone and F. solani had significantly fewer leaves (juglone × Fusarium effect, F = 7.90, P = 0.0057), shorter total root length (F = 11.06, P = 0.0013), and exhibited more root browning (F = 14.91, P = 0.0003) than plants challenged only with juglone, but there was variability among repetitions and in the development of leaf symptoms. Field and controlled environment observations point to an association, previously unreported to our knowledge, among F. solani, black walnut, and soybean disease. Tolerance of the pathogen to juglone and soybean stunting due to juglone are also novel findings, but more data are needed to conclusively prove the link with the allelopathic compound.