The proposal of abnormal activation of the eIF2α pathway has led to the recognition that activation defects of this pathway may be important modifiers of the cellular phenotype of TorsinA dysfunction in cell models, and it has been demonstrated that eIF2α dysfunction is present in fibroblasts of patients with DYT- TOR1A dystonia (Beauvais et al., 2016, 2019). The gene discussed is TOR1A; the disease is Dystonia.