To test a possible role of Cdk5-mediated Acn phosphorylation in this context, we used two different Drosophila Huntington’s disease models expressing huntingtin-polyQ polypeptides in the eye, either through GMR-Gal4-driven expression of UAS-Htt.Q93 (Figure 8B,C) or through a direct fusion of Htt-Q120 with the GMR enhancer/promoter region (GMR-Htt.Q120, Figure 8D,E). This evidence concerns the gene ACIN1 and juvenile Huntington disease.