Genome-wide association studies (GWAS) of asthma have yielded exciting results and identified novel risk alleles and loci. But, like other common complex diseases, asthma-associated alleles have small effect sizes and account for little of the prevalence of asthma. In this review, I discuss the limitations of GWAS approaches and the major challenges facing geneticists in the post-GWAS era and propose alternative strategies to address these challenges. In particular, I propose that focusing on genetic variations that influences gene expression and using cell models of gene-environment interactions in cell types that are relevant to asthma will allow us to more completely characterize the genetic architecture of asthma.
Keywords: asthma; epigenomics; gene-environment interaction; genetic variation; quantitative trait loci.