Although the length of the CAG-encoded polyQ tract seems to directly correlate with disease severity and Htt protein aggregation propensity (2, –, 4), other sequence features, including post-translational modifications (PTMs), have been shown to influence the aggregation, cellular properties, and toxicity of HTT and therefore may contribute to HD pathogenesis (5, –, 11). This evidence concerns the gene HTT and Huntington disease.