In HD, the aggregation-prone polyQ-expanded Htt protein shows stronger interaction with ribosomal proteins than its soluble wild-type counterpart, inducing dose-dependent inhibition of global translation that is likely to result from a combination of defective ribosome biogenesis and ribosomal stalling/collision during elongation (Aviner et al, 2024; Culver et al, 2012; Eshraghi et al, 2021; Kim et al, 2016). This evidence concerns the gene HTT and Huntington disease.