Findings from this GWA study provide insight into the allelic architecture of predisposition to lung cancer. Pooling data from our study with two other GWA studies provided a combined analysis of 7,560 cases and 8,205 controls. Nevertheless we have failed to identify additional loci to 5p15.33, 6p21.33 and 15q25.1. As our power to detect the major common loci conferring risks of 1.2 or greater was high we consider that there are unlikely to be many additional SNPs (tagged by the Illumina 550K array) with similar effects for alleles with frequencies > 0.2 in populations of European ancestry. Inevitably we had low power to detect alleles with smaller effects and/or MAFs < 0.1. By implication, variants with such profiles may represent a much larger class of susceptibility loci for lung cancer and current GWA based strategies based on the currently available commercial arrays are not optimally configured to identify low frequency variants with potentially stronger effects. Thus there may a large number of low penetrance variants that remain to be discovered. Further efforts to expand the scale of GWA meta-analyses, in
