Several groups assumed early on that altered histone acetylation might contribute to HD when scientists discovered that histone acetyltransferases (HAT), such as CBP, were recruited into mHtt aggregates, and an HDAC inhibitor increased histone acetylation; thus, improving the phenotype in several animal models of HD (Steffan et al., 2001; Chuang et al., 2009). Here, CREBBP is linked to Huntington disease.