Maize, an important food and commodity crop worldwide, can be infected by the fungal pathogen Fusarium verticillioides. F. verticillioides causes the disease Fusarium ear rot (FER) and produces the toxic fungal secondary metabolite (mycotoxin) fumonisin, which can reduce yields and marketability of maize grain. More importantly, fumonisin exposure is associated with health risks for humans and animals. This dissertation aimed to dissect the genetics and mechanisms conferring resistance to FER and fumonisin contamination in maize. Employing point and inundative F. verticillioides inoculation methods with a panel of 50 maize inbred lines, the symptomatology of F. verticillioides infection (FVI) was dissected, showing that kernel bulk density is an accurate predictor of fumonisin contamination in maize kernels. Quantitative trait locus mapping and correlation analyses further demonstrated the link between kernel bulk density and resistance to FVI and revealed the diverse modes of pathogenesis and resistance loci present in four tropical-by-temperate recombinant inbred line maize families. Inter-trait correlation analyses, genome-wide association mapping, and genomic prediction of 29 publicly available disease resistance (including FER) and morphophysiological traits on the maize core diversity panel revealed that height and inflorescence traits were associated and shared loci disease resistance.