Approaches to assessing power of genome wide association have used a variety of assumptions about the frequencies of disease-causing alleles, the heterogeneity and penetrance of disease-causing alleles, marker frequencies, and the nature and distribution of linkage disequilibrium across the genomic intervals surveyed [128, 129]. Many approaches to this problem use linkage disequilibrium distributions identified in HapMap samples, even though these HapMap individuals represent only very small subsets of several current human populations.
