CASP6 and Huntington disease: Studies in mice expressing a caspase-6-resistant form of mutant HTT suggest that HTT proteolysis specifically at 586 may be critical to HD pathogenesis (Graham et al., 2006; Warby et al., 2009), and overexpression of transgenic-expanded repeat HTT 586 supports potential toxicity of this fragment (Waldron-Roby et al., 2012).