As many complex disease and expression phenotypes are the outcome of intricate perturbation of molecular networks underlying gene regulation resulted from interdependent genome variations, association mapping of causal QTLs or expression quantitative trait loci must consider both additive and epistatic effects of multiple candidate genotypes. This problem poses a significant challenge to contemporary genome-wide-association (GWA) mapping technologies because of its computational complexity. Fortunately, a plethora of recent developments in biological network community, especially the availability of genetic interaction networks, make it possible to construct informative priors of complex interactions between genotypes, which can substantially reduce the complexity and increase the statistical power of GWA inference.