Evidence from animal PRRT2 models suggest that local cerebellar hyperexcitability would be sufficient to generate involuntary dyskinesia (58) resembling the PKD phenotype in humans, learning difficulties (59) as observed with patients carrying biallelic PPRT2 mutations, and, to some extent, also an epileptic susceptibility (46). The gene discussed is PRRT2; the disease is drug-induced dyskinesia.