The idiopathic generalized epilepsies (IGEs) are considered to be primarily 
genetic in origin. They encompass a number of rare mendelian or monogenic 
epilepsies and more common forms which are familial but manifest as complex, 
non-mendelian traits. Recent advances have demonstrated that many monogenic IGEs 
are ion channelopathies. These include benign familial neonatal convulsions due 
to mutations in KCNQ2 or KCNQ3, generalized epilepsy with febrile seizures plus 
due to mutations in SCN1A, SCN2A, SCN1B, and GABRG2, autosomal-dominant juvenile 
myoclonic epilepsy (JME) due to a mutation in GABRA1 and mutations in CLCN2 
associated with several IGE sub-types. There has also been progress in 
understanding the non-mendelian IGEs. A haplotype in the Malic Enzyme 2 gene, 
ME2, increases the risk for IGE in the homozygous state. Five missense mutations 
have been identified in EFHC1 in 6 of 44 families with JME. Rare sequence 
variants have been identified in CACNA1H in sporadic patients with childhood 
absence epilepsy in the Chinese Han population. These advances should lead to 
new approaches to diagnosis and treatment.