Most genome-wide association studies rely on single nucleotide polymorphism (SNP) analyses to identify causal loci. The increased stringency required for genome-wide analyses (with per-SNP significance threshold typically approximately 10(-7)) means that many real signals will be missed. Thus it is still highly relevant to develop methods with improved power at low type I error. Haplotype-based methods provide a promising approach, however, they suffer from statistical problems such as abundance of rare haplotypes and ambiguity in defining haplotype block boundaries.