In PKD patients with PRRT2 mutations, it is presumed that abnormal cerebellar output is the primary dysfunction, which leads to striatal dysregulation and paroxysmal dyskinesia.[10] In PRRT2‐deficient mice, dyskinetic movements were triggered due to the induction of cerebellar spreading.[11] However, global characterization of PKD‐associated neural disruptions, especially the functional connectivity, is still lacking.[12, 13, 14, 15]. The gene discussed is PRRT2; the disease is paroxysmal dyskinesia.