has been implicated in ASD aetiology based on observations of multiple de novo SNVs [65–67]. FOXP1 has also been implicated in several related cognitive phenotypes including language impairment and intellectual disability [68–70]. Moreover, in a murine Foxp1 KO mouse model, in addition to observable neuronal phenotypes, mice exhibit many behavioural phenotypes associated with ASD [71]. The genetic relationship we observed for common variation shared between schizophrenia and ASD is striking; alongside shared rare structural variation, such as that observed in the 22q11.2 deletion syndrome [72], these data suggest a common risk and a shared biology leading to related but distinct outcomes. We must also consider potential confounding; there is some evidence to support increased assortative mating within and across psychiatric illnesses. Consequently, the evidence from a cross-disorder meta-analysis may not be due to pleiotropy (or not entirely) but may instead be an artefact of a residual genetic background from assortative mating between individuals with these diagnoses [73]. Whether the observed degree of such assortative unions can explain the observed correlations will require further investigation.
