were genetic in origin. The underlying disease model contained four major genes and two modifier genes. The four major genes interacted with each other to produce three different "phenotypes", which were themselves heterogeneous. The population parameters were calibrated so that the major genes could be discovered by linkage analysis in most datasets. The association evidence was more difficult to calibrate but was designed to find statistically significant association in 50% of datasets. Some linkage disequilibrium between marker loci was simulated around some of the genes and also in areas without disease genes. Data distributed to participants contained about 1,000 SNPs and 400 microsatellite markers. Data obtainable via the internet consisted of a finer 10,000 SNP map, which also contained data on controls. These data are described in detail in Greenberg et al. [2].
