Put together, our results indicate that a combination of GWAS and functional molecular data on a genome-wide scale can be used to uncover additional disease-related genes with likely small-effect sizes. This approach can be easily adapted to many phenotypes, the major limitation being the availability of suitable samples for the expression studies. Going forward, it will be important to apply this approach to a variety of intermediate quantitative phenotypes relevant to asthma and other diseases sharing a dependence on lymphocytes for their pathogenesis.
