part of 321 ISSN 1758-2008 10.2217/NPY.13.25 © 2013 Future Medicine Ltd Neuropsychiatry (2013) 3(3), 321–330 Neuropsychiatry (2013) 3(3), 321–330 SUMMARY Gilles de la Tourette syndrome (GTS) is a neuropsychiatric disorder of childhood onset, characterized by the presence of multiple motor and phonic tics. Early twin and family aggregation studies have suggested that genetic factors play a critical role in the development of GTS. However, identifcation of causative mutations and susceptibility regions has proved difcult. This may be attributed to various factors, including the clinical heterogeneity of GTS, the presence of comorbid psychopathology, gene–environment interactions and bilineal transmission. This review assesses the diferent methodologies of genetic studies with explanatory comment for the clinician, and summarizes key genetic fndings in light of their potential implications for treatment strategies. 1 Department of Neuropsychiatry, BSMHFT & University of Birmingham, Birmingham, UK 2 School of Clinical & Experimental Medicine, University of Birmingham, Birmingham, UK 3 Neurosciences Department, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK 4 Department of Neurology, University Hospitals Birmingham NHS Foundation Trust & University of Birmingham, Birmingham, UK 5 School of Life & Health Sciences, Aston University, Birmingham, UK 6 Sobell Department of Motor Neuroscience & Movement Disorders, Institute of Neurology & University College London, London, UK *Author for correspondence: a.cavanna@ion.ucl.ac.uk REVIEW Fizzah Ali 1,2 , Karen E Morrison 3,4 & Andrea E Cavanna* 1,5,6 The complex genetics of Gilles de la Tourette syndrome: implications for clinical practice Practice points  Gilles de la Tourette syndrome (GTS) is a neurodevelopmental condition characterized by the presence of multiple motor and phonic tics.  The clinical picture of GTS is heterogeneous, ranging from simple tics to complex behaviors, frequently associated with psychiatric comorbidity.  Once considered a rare condition, GTS is now estimated to afect 0.4–3.8% of school-age children.  Since twin and family aggregation studies have suggested that there is a signifcant genetic basis to GTS, a wide range of genetic methods have been employed to elucidate the genetic architecture of GTS.  Detailed consideration of clinical phenotypes and improved characterization of study populations may aid in delineating genetic loci in symptomatically homogeneous groups and developing tailored treatments.  We anticipate that further investigation into the basis of genetic susceptibility in GTS will improve our understanding of its pathophysiology and guide the development of efective treatment strategies.