Single nucleotide polymorphisms (SNPs) were selected for analysis with a bias toward variants for T2D and glucose homeostasis traits (e.g., fasting glucose), which have exhibited relatively large effect sizes and which have been widely replicated. This resulted in the selection of 57 variants (23 (link)–27 (link)) for analysis. Based on the a priori evidence of association, this discovery set yields increased power as well as increased probability of detecting effects across ancestries. Genotyping and quality control have been described in detail (22 (link)). Briefly, samples were genotyped on the Illumina HumanOmniExpress array. Samples with call rates >0.98 and SNPs with call rates >0.99 and minor allele frequency >0.001 passed laboratory quality control following usual best practices (e.g., sufficient signal and cluster separation with no replicate errors) (28 (link)). For family-based studies, pedigree structures were confirmed using standard procedures (e.g., Kinship-based INference for Gwas [KING] [http://people.virginia.edu/∼wc9c/KING/index.html]), and SNPs were examined for Mendelian inconsistencies using PedCheck (http://watson.hgen.pitt.edu/register/docs/pedcheck.html).