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That type 1 diabetes in humans and in animalmodels represents a complex genetic disease isuniversally accepted. Genetic dissection of type1 diabetes in humans has typically entailed the collection of large numbers of individuals scored on the basis of the presence or absence of clinical disease (case/ control subjects). Statistically significant differences in allele frequencies distinguishing the affected subjects from control subjects are used to demonstrate associations. Human major histocompatibility complex (MHC) alleles, primarily but not exclusively within the class II sets of genes, are estimated to contribute up to 50 % of genetic risk. Because of the strength of the MHC contribution and the genetic heterogeneity extant in humans, identification of non-MHC susceptibility loci by genome-wide association has required the accumulation of large numbers of case/control populations. Recent studies have identified up to 10 of such non-MHC susceptibility regions under conditions where mul