The identification of similar eIF2α dysregulation and synaptic plasticity defects as previously described in DYT1 mice and rats in the DYT6 animals is a key convergence of biological mechanisms among inherited dystonias, perhaps adding the group of translational dysregulation-associated dystonias (DYT1, DYT3, DYT6, and perhaps DYT16 [24,26,80] to those linked to dopamine dysfunction (DYT5, DYT11, DYT25) [7]. The gene discussed is TOR1A; the disease is Dystonia.