The assumption that altered histone acetylation might contribute to HD was made in the early 2000s, when it was found that the HAT CREB-binding protein CBP is recruited into aggregates of mutant Htt, and that HDAC inhibitors (HDACi) improve phenotypes of drosophila and mouse models of HD (Nucifora et al., 2001; Steffan et al., 2001; Kazantsev et al., 2002). Here, HTT is linked to Huntington disease.