Moreover, preferential expression of either the mutant or wild-type allele is another possible explanation for the incomplete penetrance of SZ risk genes (reviewed in ref. 11); indeed a study of allele-biased expression in hiPSC-derived neurons identified putative SZ and autism spectrum disorder-associated genes, including CNTNAP2, to be robustly implicated in allele-biased expression.12 Although the mechanistic effectors remain unidentified, here we present evidence that differences in both exon- and allele-specific expression may have a critical role in SZ predisposition. The gene discussed is CNTNAP2; the disease is autism spectrum disorder.