The widespread application of genome-wide association studies (GWAS) has contributed to a revolution in the research of human genetics and the genetic determinants that underlie complex disease. A recent study suggested that selecting genetically supported therapeutic targets implicated by GWAS could potentially double the success rate in the clinical development of new pharmaceutical treatments [1]. While GWAS have identified thousands of genetic variants associated with human complex traits and diseases, there are still several important limitations to these prevailing types of genetic association studies [2,3]. A longstanding challenge of GWAS lies in exploring the mechanisms by which these genetic loci affect the variation of complex traits and the pathophysiology of complex diseases.
