THAP1 and Dystonia: In conclusion, the differentiation of patient-derived iPSCs toward MSNs provided a feasible in vitro model of DYT-THAP1 dystonia and gave insights into the functional phenotype with altered intracellular calcium dynamics, increased calcium amplitudes after application of acetylcholine, reduced GABA-evoked calcium signals, inhibited synaptic activity and enhanced postsynaptic generation of action potentials.