Indeed, by taking into consideration that mono-ubiquitinylation is involved in modulating protein function, compartmentalization, and interactions, while polyubiquitinylation is a signal for protein degradation [71,72], collectively, the results suggest that more than the expression levels, the regulation of BACH1 activity/degradation plays a role in DS and contributes to the explanation of observed changes with regard to HO-1 [6]. Here, BACH1 is linked to Dravet syndrome.