It is unlikely that torA-ΔE expression completely ablates LINC complex activity, as genetic deletion of the complex in mice results in severe neurodevelopmental abnormalities [23], compared with undetectable or limited neuropathology in human DYT1 dystonia patients and heterozygous torA-ΔE expressing mice [41]. Here, TOR1A is linked to early-onset generalized limb-onset dystonia.