Animal models of dystonia forms with reduced or incomplete penetrance, such as DYT-TOR1A, DYT-THAP1, DYT-GNAL, DYT/PARK-GCH1, DYT/PARK-TH and DYT-SGCE, offer the opportunity to study the pathophysiological mechanisms leading to the expression of a dystonic phenotype. This evidence concerns the gene THAP1 and Dystonia.