From 2007 to 2015, genome-wide association studies (GWAS) resulted in the discovery of over 260 genetic loci associated with obesity and type 2 diabetes (T2D) (1,2). Although GWAS have validated “old culprits” (e.g., PPARG , KCNJ11 ), illuminated novel disease-causing biological pathways (e.g., the zinc transporter SLC30A8 ), and have led to quick translational medicine applications (e.g., hs-CRP as a diagnostic tool for HNF1A maturity-onset diabetes of the young) (3–5), some have questioned their utility (6,7). They argue GWAS are expensive and that GWAS-derived single nucleotide polymorphisms (SNPs) explain only a fraction of the heritability for complex traits (6,7). They propose to focus instead on next-generation sequencing (NGS) studies or post-GWAS experiments (functional studies, animal models, clinical studies) (6,7). This debate has led to skepticism about the benefits of GWAS and hesitancy to fund additional GWAS. With the ever-decreasing costs in NGS technologies, we should seriously address the relevance of funding more GWAS. In this issue of Diabetes , Scott et al. (8) provide some elements of response to this important question. The authors conducted a meta-analysis of 18 GWAS totalling 26,676 T2D case and 132,532 control subjects. They imputed 12.1 million SNPs using the multiethnic 1000 Genomes Project (1000G) reference panel. Twenty-nine SNPs showing promising associations ( P < 10−5) with T2D in the stage 1 GWAS were …