KCTD17 mRNA was shown to be broadly expressed across the brain but particularly in the putamen, consistent with dystonia being caused by dysfunction of basal ganglia circuits.79 Fibroblasts derived from a KCTD17 patient (p.Arg145His) exhibit defective ER calcium signaling, which is suggested to underlie myoclonus‐dystonia linked to mutations in other genes (e.g., HPCA, CACNA1A, ANO3).79, 83. This evidence concerns the gene KCTD17 and Myoclonus.