BACH1 and Dravet syndrome: Increased BACH1 protein levels along with reduced BACH1 mono-ubiquitinylation would be responsible for the lack of HO-1 or NQO1 increase observed in DS, while increased BACH1 poly-ubiquitinylation (degradation) would drive the observed increase of HO1 and NQO1 protein levels in DSAD persons [6].