Importantly, the Hayden lab found that overexpressing the HTT S-acylating enzyme ZDHHC17 or pharmacological inhibition of the HTT deacylating enzymes APT1 and APT2 increases mutant HTT S-acylation, reduces its aggregation, and rescues neurotoxicity in multiple cellular models, including neurons from HD mouse models (Lin and Conibear, 2015; Lemarié et al, 2021). This evidence concerns the gene HTT and Huntington disease.