Mouse models may be useful in helping to understand the functional consequences of these variants. The reverse may also be true: these rare structural variants may turn out to be more valuable than the originally identified common variant in establishing a link between ZNF804A and a psychosis-related phenotype in an animal model. This is because gene knockout or overexpressing mice can be engineered relatively easily, the penetrance of pathogenic CNVs is generally much higher than common SNP variants, and temporal or cell specific manipulation of expression can be carried out with conditional mutants.
