Increased p62 levels that indicate autophagosome-lysosome fusion step impairment (and consequent absence of the cargo degradation) have been observed in some neurodegenerative disorders characterized by accumulation of protein aggregates, including Lewy bodies (in Parkinson’s disease), neurofibrillary tangles (in Alzheimer’s disease), Huntingtin aggregates (in Huntington’s disease), and Mallory bodies (in alcoholic and nonalcoholic steatohepatitis) [52,53,54]. The gene discussed is HTT; the disease is metabolic dysfunction-associated steatohepatitis.