After Doose et al.  described epilepsy with myoclonic-atonic seizure (MAE), exploration of genetic causes has been ongoing . Recent studies have identified pathogenic variants in SLC2A1 and SLC6A1 in 4% and 5% of MAE patients, respectively [3,4]. SLC2A1 has also been identified as responsible for up to 10% of early onset absence epilepsy (EOAE) patients [5–7]. Similarly, EOAE and childhood absence epilepsy have also been reported in patients with pathogenic variants in SLC6A1 . Therefore, although the principal seizure type may characterize MAE and EOAE as distinct epilepsy syndromes, they may share a genetic etiology.