DAT-KO mice can be used as a model of DTDS because they share a genetic background and the absence of DAT functionality, accompanied by a set of phenotypic features that are strikingly reminiscent of DTDS symptomatology, including hyperkinesia at early stages, followed by the progression of motor impairment, hypokinesia/dyskinesia and dorsal kyphosis5, 17, 18. The gene discussed is SLC6A3; the disease is SLC6A3-related dopamine transporter deficiency syndrome.