Recent genome-wide association studies (GWAS) have identified loci that harbor susceptibility genes for asthma and other pulmonary conditions [1]–[16]. Many of the genes at these loci have unknown function and have not previously been considered biologically plausible candidates for disease pathogenesis. Extensive linkage disequilibrium (LD) within these loci makes it difficult to identify the actual susceptibility genes, let alone which genetic variants are responsible for altered expression or function of their protein products. Moreover, the associated polymorphisms can only explain a relatively small proportion of the variability of the phenotype in the population [9] and of its heritability [17].
