In addition, the mutant HTT leads to both reduced DHHC17 interaction and activity, potentially resulting in reduced palmitoylation and DHHC17 substrate (e.g., GAD65, SNAP25, SYT1, and PSD95) mislocalization, ultimately aggravating HD pathogenesis [48, 90, 100, 124]. This evidence concerns the gene DLG4 and Huntington disease.