There remains a pressing need to understand the initiation, propagation, and termination of seizures at the network level in different forms of epilepsy in order to devise better treatment strategies. Understanding how neuronal synchrony within a microcircuit reaches a critical threshold, subsequently allowing it to entrain larger populations of neurons, could suggest novel mechanisms that can be engaged to terminate a seizure. Although there are volumes of work on this topic over the decades,9-11 new advances in stratification of epilepsies through pharmacogenomics12 and genetic analysis13 could provide new understanding of mechanisms in models relevant for human disease. Advances in computational models have reached the point where both interictal and ictal activities can be reliably generated from the same network. The predictions of these models can now be practically verified.14,15 Additional insights may also follow from a determination of the relative contribution of shared cellular and network mechanisms to different models. Similarly, advances in modeling the process of epileptogenesis suggest interesting new mechanisms, yet highlight the complexity of the problem.16 These mechanisms could lead to the testing of more effective therapies.