CREBBP and Rubinstein-Taybi syndrome: Wang et al. showed that CBP haploinsufficiency or CBP knockdown inhibited the differentiation of embryonic cortical precursors into neurons, astrocytes, and oligodendrocytes, coinciding with a decrease in CBP binding and histone acetylation (H3K9/14 acetylation) to neuronal and glial gene promoters such as α1-tubulin, Gfap, and Mbp. The CBP defect caused early cognitive dysfunctions, such as Rubinstein-Taybi syndrome.68 CBP/p300 also determines the cell lineage specificity in an activator-dependent manner.