Given that the transcriptional activity of the FOXO3/ß-catenin complex is central to neuronal compensation in HD and that FOXO3 neuroprotection is altered during the early phases of the HD process6, 9, 11, 18, 23, these compounds —or similar compounds with better brain prodrug properties— could enable an efficient level of FOXO3 neuroprotection to be ensured in HD and the functional longevity of HD neurons to be prolonged. This evidence concerns the gene FOXO3 and Huntington disease.