OLIG2 and Dravet syndrome: Moreover, the commitment and lineage development of inhibitory neurons are PRC2-dependent [132, 243] and while OLIG2 is triplicated in DS, it is also known to be highly regulated by HMGN1 [121], suggesting that despite the above discrepancy between the studies, there is a consistency in reported deficits in the interneuron motility and the disbalance between the excitatory and inhibitory neurons that can be potentially caused by the gene dosage of HMGN1 and subsequent dysregulation of PRC2 targets.