Huntington’s disease is a rare neurodegenerative disorder, affecting an estimated 1 in 10,000 individuals worldwide. It is characterized by a range of motor, cognitive, and psychiatric symptoms. Motor symptoms include involuntary movements, difficulties with coordination and balance. Cognitive symptoms manifest as impairments in memory, executive function, and attention. Psychiatric symptoms may include depression, anxiety, irritability, and personality changes. The age of diagnosis typically ranges from 30 to 50 years, with some cases occurring earlier or later in adulthood. While its prevalence may be low, the impact of HD is significant and far-reaching, affecting not only those living with the disease but also their families, healthcare systems and society as a whole. Currently, no disease-modifying therapies are available for HD, and the average life expectancy following diagnosis is only 15-20 years. Understanding the mechanisms of HD and developing effective treatments is therefore crucial to improve the lives of affected individuals. The present study aims to contribute to this effort by shedding light on the role of mutant HTT gene transcripts in cellular toxicity. By identifying proteins sequestered in RNA foci, we could potentially discover therapeutic targets to prevent or reverse the toxic effects of these transcripts. The findings of this study could lead to the development of novel HD treatments targeting underlying cellular mechanisms. Such treatments could enhance the quality of life for patients and their families, reduce the economic burden of caring for HD patients, and advance our understanding of the cellular and molecular mechanisms of neurodegenerative diseases more broadly.