A comprehensive investigation of the underlying genetic architecture of type 2 diabetes has unveiled the most detailed look at the genetic differences that heighten a person’s risk for disease development. The findings, published today in the journal Nature by an international team of more than 300 scientists led by the University of Oxford, the Broad Institute, and the University of Michigan, reveal the complexity of the disease in more detail than previously appreciated, but also identify several promising targets for new treatments. Using DNA sequencing in more than 120,000 people with ancestral origins in Europe, South and East Asia, the Americas and Africa, the authors, including Francis Collins, M.D., Ph.D., director of the National Institutes of Health and head of the Molecular Genetics Section at the National Human Genome Research Institute, evaluated the genome at a greater level of detail than had been previously attempted for type 2 diabetes. Some individuals had their entire genome sequenced while for others the researchers focused on the part of the genome that codes directly for proteins, known as the exome. The researchers then compared the genetic changes between affected and healthy participants. The findings suggest that most of the genetic risk of type 2 diabetes can be attributed to common, shared genetic variants – each contributing a small amount to an individual’s risk of the disease – rather than many rare variants unique to individuals. This resolves a question about the genetics of type 2 diabetes that has puzzled researchers for decades.