Overexpression of FOXO3, but not that of FOXO3‐TM (a nonphosphorylatable mutant), decreased ETS2 and p16INK4a mRNA levels in human HD NSCs subjected to growth factor deprivation (Figure 3c), suggesting that nucleo‐cytoplasmic shuttling of FOXO3 is required for repressing ETS2 and for ensuring homeostasis of interactions with potential co‐repressors (van der Vos & Coffer, 2008), also suggesting that increased FOXO3‐binding to the ETS2 promoter is part of the general increase of FOXO3 binding in HD NSCs. Here, ETS2 is linked to Huntington disease.