(with 80% accuracy for coronary artery disease, for instance). Notably, they were also able to identify subsets of the testing sample with odds ratios of 3, 4, or 5 for having illness. This is comparable to the predictive ability of many monogenic mutations in Mendelian diseases. The group of subjects this applied to was small (for the five diseases, the size of this risk group ranged from the top 1.5% to the top 8.0% of subjects with the highest PRS), but for those groups the PRS might have some clinical utility even now. There is no reason that this method cannot be applied to common psychiatric disorders and it is supported by data showing that subjects with a top-decile PRS for schizophrenia have a threefold increased risk of psychosis 25 and a further study showing that the top-decile PRS for major depressive disorder was associated with a 2.5-fold increased risk of major depression 26. Of course, the relevant question in a clinical situation is usually not to differentiate between typical cases and symptom-free controls but to identify individual cases who might benefit from specific treatments. We would anticipate that young at-risk individuals with a high PRS might benefit from psychoeducation,
