Given the significant positive correlation between circHomer1a and the age of onset of SCZ in both the OFC and DLPFC (the earlier the onset the more robust the reduction in circHomer1a) and the alteration on numerous mRNA isoforms strongly linked to psychiatric disease and control of neuronal function, such as Psma4, Fmr1, and Cacnb4, it is tempting to hypothesize that deficits in circHomer1a within the PFC could contribute to the disturbances in synaptic plasticity and glutamatergic neurotransmission that have been observed in SCZ [4–8]. Here, FMR1 is linked to psychiatric disorder.