Thornton et al. [2013] found that the association analysis of the first simulated replicate of DBP across the odd autosomes using PLINK, where with the top PCs from a PCA with the EIGENSOFT software were included as covariates, lead to systematically inflated p-values. The genomic control inflation factor [Devlin and Roeder, 1999], λ, was 1.3 as a result of unaccounted population and pedigree structure. In contrast, λ =0.97 for the association analysis with the EMMAX, indicating that the method is slightly conservative for the GAW18 data. EMMAX identified genome-wide significant associations for SNPs in the MAP4 gene on chromosome 3. This gene is causal for the simulated DBP phenotype.
