Up to now, mutations in the GABRG2 gene, encoding the GABAA receptor γ2 subunit, have been reported in a subset of families, but their prevalence remained unknown. In the literature, individuals with GABRG2 mutations presented a variety of phenotypes ranging from pure FS,22 FS+ or FS and generalized epilepsy (absence seizures or GTCS),7,20,23–29 GTCS without FS,30 FS and rolandic epilepsy,31 to possibly Dravet syndrome (a nonsense mutation was reported in dizygotic twins with Dravet syndrome and their healthy father).32