We develop a population genetics model for the northern corn rootworm, Diabrotica barberi Smith & Lawrence, to examine the effect of extended diapause on the evolution of resistance to transgenic Bacillus thuringiensis (Bt) corn, Zea mays L. We model conditions found in the center of the extended diapause problem along the Minnesota–South Dakota–Iowa borders. The proportion of resistance alleles in eggs oviposited after 15 simulated years is used to measure the evolution of resistance. Sensitivity analysis indicates that although population genetics parameters (fecundity, initial egg density, density-dependent larval survival, random mating, insecticide mortality, and gene expression) affect the evolution of resistance, product characteristics (e.g., Bt toxin dose) and farmer management practices (e.g., insecticide use on refuge corn and rotation pattern) generally have a larger impact on the development of resistance. Exceptions to this generalization exist: 1) if the resistance allele is dominant, resistance evolves quickly; 2) the level of random mating is an important determinant of how quickly resistance evolves for a theoretical high dose product; and 3) small differences in insecticide mortality imply large differences in resistance for medium- and low-dose products with high levels of Bt corn adoption and a predominance of 1- and 2-yr corn rotations. When extended diapause spreads into a new area, it typically reduces resistance to Bt corn, assuming Bt corn is used only on continuous corn. In the study region where extended diapause already exists, increasing extended diapause (increasing hatch rates after two or three winters while holding total hatch constant), tends to increase resistance because the resistance increasing effect of the hatch rate after two winters dominates the resistance decreasing effect of the hatch rate after three winters. However, this is not always the case, because combinations of rotation pattern, toxin dose, and soil insecticide use exist for which the net effect of extended diapause decreases resistance. Results are interpreted as a combination of two offsetting effects. First, extended diapause injects older alleles with lower resistance allele frequencies into the breeding population, which slows resistance. Second, extended diapause speeds the population’s recovery from perturbations (reduces the undercompensating density dependence of population dynamics), which accelerates resistance.