In agreement with our previous analysis of the effects of the phosphomimetic AcnS437D mutant (Nandi et al., 2017), all three methods yielded increased pS437-Acn levels which elevated autophagic flux, as indicated by improved clearance of polyQ load in a Drosophila model of Huntington’s disease, or the increased number of ATG8-positive autophagosomes and autolysosomes without concomitant p62/Ref(2)p accumulation. Here, ACIN1 is linked to Huntington disease.