From a different perspective, Greenwood et al. (3) used a genetic approach to tap the genome, which because of the moderate to high heritability of schizophrenia is a proven reserve of information on the origins of this disease. Taking advantage of the deep neurocognitive phenotyping in the Consortium on the Genetics of Schizophrenia (COGS), this multicenter team detected genetic associations to 12 schizophrenia-related neurocognitive traits, several of which are strongly influenced by frontal function. Among their 96 candidate genes, and taking into account a total of 16,620 tests due to analysis of 1,385 single-nucleotide polymorphisms (SNPs) and 12 endophenotypes, Greenwood et al. found 30 SNPs with p values <0.001. Of the 96 genes, 23 were implicated at this level, far more than would be expected by chance. Most strongly represented were GABA/glutamate genes. Such neurocognitive systems approaches are probably critical for diseases such as schizophrenia, in which there is substantial genetic heterogeneity and where risk alleles may reside in different genes within the same network. Indeed, the schizophrenia genes identified so far as copy number variants have been rare, and there appear to be many genes involved. Because schizophrenia is common and clinically defined, we may perfectly reasonably expect that one day it will be retrospectively viewed as an amalgam of many distinct disorders that are individually much less common. By analogy, schizophrenia is at the state of hereditary deafness or anemia, both of which were syndromes without known causes prior to 20th-century medicine.