Heterozygous animals carrying the DYT1 dystonia mutation in the TOR1a gene exhibit no behavioral defect, but defects in the cerebello-cortical pathway are similar to those found in human non-manifesting gene carriers, confirming the role of this pathway in the penetrance of the disease (Uluğ et al., 2011). This evidence concerns the gene TOR1A and early-onset generalized limb-onset dystonia.