In the largest molecular genetic study of schizophrenia ever conducted, or indeed of any neuropsychiatric disorder, we demonstrate the power of GWAS to identify large numbers of risk loci. We also show that the use of alternative ascertainment and diagnostic schemes designed to rapidly increase sample size does not inevitably introduce a crippling degree of heterogeneity. That this is true for a phenotype like schizophrenia where there are no biomarkers or supportive diagnostic tests provides grounds to be optimistic about applying GWAS to other disorders where diagnosis is similarly clinician-based, and recruitment traditionally constrained by the need for expensive and time consuming assessments.
