Height has been used as a model trait for the study of human polygenic traits, including common diseases, because of its high heritability and relative ease of measurement, which enable large sample sizes and increased power. Conclusions about the genetic architecture, sample size requirements for additional GWAS discovery and scope for polygenic prediction that were initially made for height have by-and-large agreed with those for common disease. If the results from this study can also be extrapolated to disease, this would suggest that substantially increased sample sizes could largely resolve the heritability attributed to common variation to a finite set of SNPs (and small genomic regions). These variants and regions would implicate a particular subset of genes, regulatory elements and pathways that would be most relevant to address questions of function, mechanism and therapeutic intervention.
