Indeed, CBP dysfunction has been identified in a number of neurological disorders, such as the Rubinstein–Taybi syndrome (RTS), AD, Amyotrophic Lateral Sclerosis (ALS) and polyQ-related diseases, in which CBP has been found in the inclusion bodies formed by polyglutamine-containing proteins in HD, DRPLA, SCA3, SCA7, and spinal and bulbar muscular atrophy (SBMA) [52–56]. The gene discussed is ATXN3; the disease is Huntington disease.