HDAC8 lacks a predicted miR-153 target site within its 3′UTR, but we examined its expression following miR-153 over-expression because it is the earliest type-1 HDAC to be expressed during neurogenesis in the fetal murine telencephalon (Murko et al., 2010) and is implicated in the etiology of the Wilson–Turner X-linked (Harakalova et al., 2012) and Cornelia de Lange (Deardorff et al., 2012) syndromes, both of which are characterized by cognitive impairment. Here, HDAC9 is linked to Cognitive impairment.