observed allelic expression imbalance was not directly attributable to rs1344706, at least in the adult brain. In fact, rs1344706 genotypes were found to have a significant effect on ZNF804A allelic expression in second-trimester fetal brain tissue, however with the SZ risk allele associated with a reduced expression (Hill and Bray, 2012). This is in contrast with our findings, but one possible explanation could be the reversal of fetal expression trajectories. It has been shown that fetal expression changes are negatively correlated with those in other stages of life, thus suggesting that select fetal expression changes are reversed at different times across the lifespan (Colantuoni et al., 2011), in fact ZNF804A general expression appears to be increased in fetal brain compared to levels found in adult prefrontal cortex. Finally, it is possible, but not likely, that rs1344706 might be indirectly related to the ASE we have observed, as it could be in LD with the unknown causal variant, or could be related to general ZNF804A expression, these possibilities will require further analysis in independent cohorts.
