To date, etiologic mouse models of DYT1 dystonia do not have any obvious dystonic features or evidence of pathology such as neuronal loss, including transgenic mice expressing human mutant torsinA (hMT) [12], [13], [14], and heterozygous knock-in mice in which the ΔGAG mutation has been introduced in the endogenous mouse Tor1a gene [15], [16]. The gene discussed is TOR1A; the disease is early-onset generalized limb-onset dystonia.