GWASs have been performed for a wide range of common diseases and traits, and over 6,000 strong SNP associations (p<10−8) have been identified.35 Variation at multiple genetic loci collectively influences the likelihood of developing many common and complex diseases; for instance, it is estimated that that about 8,300 independent and predominantly common SNPs contribute to risk for schizophrenia46 (MIM: 181500). Although the genetic architecture is likely to differ for different diseases, often the trait architecture consists of a few loci of relatively large effect and many additional loci that have a very small effect on phenotype.47 To understand the genetics of complex disease, it is important to consider the phenotypic and genetic overlap among diseases. For instance, susceptibility loci that are common to both multiple ulcerative colitis and Crohn disease have been identified by GWASs, and some of these loci are even shared with several other autoimmune disorders.48 Similarly, several psychiatric disorders share risk loci.49 The study of the distribution of overlapping loci within a group of diseases might suggest shared pathways and common pathogenetic features.23 On the other hand, the lack of overlap of other loci could help to identify pathogenic mechanisms that are unique to specific diseases and could help to explain phenotypic diversity across the spectrum of diseases in fields such as autoimmunity or psychiatry.50 The computational resources presented here offer a tool for comprehensively measuring the phenotypic overlap of a wide range of common diseases that share risk loci.