in lymphoblastoid cell lines (LCLs) from a set of asthmatic probands, their parents and siblings, was intersected with the GWAS data, resulting in the implication of ORMDL3 as a novel childhood asthma susceptibility gene (12). In this case, the integration of functional data also suggested that regulatory variation impacting the expression level of ORMDL3 was the likely risk-conferring mechanism for the associated variants. While subsequent studies have shown that the regulation of nearby genes, such as GSDML, may also be affected by the variant, the principle mechanism of regulatory variation influencing gene expression levels has not been challenged (13–16).
