While the relationships between impaired neurogenesis and inhibitory interneuron deficits in the prefrontal cortex and striatum remain to be examined, decreased ASCL1, DLX6-AS1 and DCX gene expression in high inflammation subgroups pinpoints altered regulation of neurogenesis in the SEZ as a possible origin of the widely reported inhibitory interneuron deficits in psychiatric disorders [10, 102]. This evidence concerns the gene ASCL1 and psychiatric disorder.