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 terms of both sample size and SNP coverage, and to increase the number of SNPs taken forward to large-scale replication may thus lead to the identification of additional variants for lung cancer. Twin studies have not however, provided evidence for heritable factors for the risk of lung cancer(15, 16). The identification of disease-causing alleles for lung cancer may thus be inherently harder than for other cancers in which familial aggregation of a major lifestyle/environmental risk factor is less likely to be a confounder.
