Although the increased FOXO3a mRNA expression demonstrated in the current study could at least partially explain its higher protein levels in HD cells, it remains possible that differential regulation of FOXO3a relative half-life/degradation in the control and mutant Htt or 3-NP stressed cells is also part of the cause, especially because we demonstrated decreased levels of pERK, which has been shown to phosphorylate FOXO3a, promoting its degradation (24). This evidence concerns the gene HTT and Huntington disease.