Whilst genetics provides the rational route to treatments which can correct the core underlying biochemical abnormalities of a heritable disorder like schizophrenia, such benefits are unlikely to be either direct or rapid. A reality check is provided by Plenge et al. (2013), who list a series of generic criteria to be considered when applying genetic findings to drug target validation (Table 2). Whilst it is a moot point whether these criteria are all valid in the context of schizophrenia, they do serve to illustrate the substantial size of the task ahead. Indeed, at present we fall at the first hurdle (and at most if not all of the others); for example, we have few if any causal variants, we merely have statistically associated tag SNPs and large CNVs, the impacts of which (as well as the relevant functions of the affected gene[s]) are at best poorly understood. Thus, it is usually not clear whether the therapeutic goal would be to enhance or decrease the actions of the implicated gene product. And, critically, since each gene independently contributes such a small
