including CNTNAP2 and ASTN2 (Tables 2 and 3). As we did not have comprehensive phenotypic data regarding social disability syndromes or psychosis in our TS cohort, it was not possible for us to assess phenotypic overlap in individuals with putatively overlapping genetic risks. However, recent findings in ASD, SCZ, ID all suggest that the diversity of phenotypic outcomes from apparently identical mutations is unlikely to be explained entirely by overt “co-morbidity” (73).
