Multiple additional lines of evidence allow us to conclude the deviation between the observed and null distributions in our primary GWAS indicates a true polygenic contribution to schizophrenia. First, applying a novel method 30 that uses LD information to distinguish between the major potential sources of test statistic inflation, we found our results are consistent with polygenic architecture but not population stratification (Extended Data Figure 3). Second, for 78% of 263 LD-independent SNPs with P <1×10−6 in the case-control GWAS, the risk alleles from were overrepresented in cases in the independent samples from deCODE (P = 5.6 ×10−21). This degree of consistency between the primary GWAS and the replication data is highly unlikely to occur by chance (P = 1×10−9). (Note the tested alleles surpassed the P < 10−6 threshold in our GWAS before we added either the trios or deCODE data to the meta-analysis. This trend test is therefore independent of the primary case-control GWAS). Third, analysing the 1,235 parent-proband trios, we again found excess transmission of the schizophrenia-associated allele at 69% of the LD-independent SNPs with P <1×10−6
