Nevertheless, two other studies in the HD mouse model showed that increasing NAD+ availability and causing SIRT-1 activation with β-lapachone (a natural o-naphthoquinone compound, and a substrate of NADH:quinone oxidoreductase, NQO1) results in neuroprotection by activating autophagy of Htt exon1-expressing cells [75,76], revealing that further investigations involving sirtuin modulators and HD are still needed. Here, HTT is linked to Huntington disease.