In another patient with comorbid tics we found a de-novo deletion of 310 kb in 12q23.1 harbouring the genes ANKS1B and UHRF1BP1 and a duplication of 80 kb in 19p13.11 harbouring the genes GMIP, ATP13A1, ZNF101 and ZNF14. ANKS1B is predominantly expressed in the brain and known to interact with the amyloid beta protein precursor that may play a role in normal brain development and in the pathogenesis of Alzheimer’s disease [69, 70]. This evidence concerns the gene ANKS1B and tic disorder.