In support of this hypothesis are the following observations: (i) abnormal plasticity and loss of synaptic downscaling at cortico-striatal synapses has been shown to be a dystonia endophenotype shared by different genetic animal models of dystonia (Martella et al., 2014; Calabresi et al., 2016; Maltese et al., 2017; Zakirova et al., 2018; Yu-Taeger et al., 2020); and (ii) ADCY5 and GNAL, two DYT genes, form part of the signalling transduction machinery in response to stimulation of dopaminergic and adenosinergic signalling in MSNs (Herve, 2011; Goodchild et al., 2013; Pelosi et al., 2017). The gene discussed is GNAL; the disease is Dystonia.