Fusarium graminearum colonizes the maize ear causing Gibberella ear rot (GER) and producing harmful mycotoxins, such as deoxynivalenol (DON) and zearalenone (ZEA), that pose a risk to human and animal health when consumed. The disease can be managed in part by breeding and planting resistant maize cultivars. Resistance to GER is a quantitative and complex trait. Evaluation of diverse germplasm to identify regions and candidate genes associated with resistance may be useful for crop improvement efforts. Screening for GER is time-consuming and costly. Thus, identifying other traits that may serve as a proxy for GER resistance may accelerate resistance breeding efforts. We hypothesized that grain phenylpropanoid content and kernel composition are genetically and mechanistically related to GER resistance. We screened a diverse set of maize inbred lines for disease severity, DON, ZEA, ferulic acid, p-coumaric acid, and several kernel composition traits. Using a genome-wide association study, we identified multiple markers associated with each phenotype and genomic regions that harbor alleles for both disease and metabolite-related phenotypes. We also identified multiple metabolic pathways associated with general biotic defense and potential detoxification. End-season ferulic acid and p-coumaric acid concentrations are not strong proxies for GER resistance, but secondary metabolites are important components of the maize-F. graminearum system. In summary, we identified candidate genes and mechanisms for GER resistance, uncovered a link between phenylpropanoid content and GER, and showed that lignin mutants are more susceptible to infection by F. graminearum.