As DBC1 is a negative regulator of SIRT1, and Dbc1 knock-out mice are viable and healthy [19], we elected to use a genetic approach to ablate DBC1 levels in R6/2 mice and investigate whether the dissociation between SIRT1 and DBC1 could increase SIRT1 activity and improve HD phenotypes. Here, SIRT1 is linked to Huntington disease.