Taken together, our finding of decreased firing rates in GPe—but close to normal rates in GPi—could be explained by dual hyperactivation of both the direct and indirect pathways in our CD patients, which is also in accordance with a current model of dystonia (Vitek, 2002): While excess direct pathway gain will decrease GPi activity, overactivation of the indirect pathway will increase GPi activity (via weakened inhibitory inputs from GPe and disinhibited excitatory projections from STN). This evidence concerns the gene GPI and Dystonia.