While caution is warranted in extrapolating from mouse models of disease, available data indicate, for example, that basal ganglia output is unlikely to change following torsinA repletion in adulthood, whereas patients with DYT1 and other etiologic forms of dystonia with long-standing symptoms benefit from the circuit-based therapy of deep brain stimulation (124, 127). This evidence concerns the gene TOR1A and early-onset generalized limb-onset dystonia.