Sequestration of CBP within nuclear polyglutamine inclusions that results in a decrease in soluble CBP and CBP-dependent transcription has also been observed in cell culture and transgenic mouse models of polyglutamine disorders like spinocerebellar ataxia type 3 (McCampbell et al., 2000; Chai et al., 2002), and Huntington's disease (Steffan et al., 2001). Here, CREBBP is linked to Huntington disease.