HTT and Huntington disease: Neuropathological studies in humans suggest that the pathogenic HD gain of function could be the formation of ubiquitinated aggregates of the N‐terminal fragment of mutated huntingtin, which is thought to occur due to enhanced cleavage and aggregation of the polyglutamine rich part of the mutant huntingtin N‐terminus (DiFiglia et al., 1997; Gutekunst et al., 1999; Li & Li, 1998; Maat‐Schieman et al., 1999; Martindale et al., 1998; Sieradzan et al., 1999; Vonsattel, 2008).