Lukasiuk et al have recently presented in abstract form and in a review article, an extension to their previous analysis of gene expression during epileptogenesis. Identification of highly represented functional classification as well as individual genes that appeared across data sets was performed with cell death and survival, neuronal plasticity and immune response as the most prominent. Seventy individual genes were identified to be consistently regulated across at least three studies using specific time-point analyses (64, 65) . Our data indicates only 22 genes consistently regulated across at least three studies. This difference is explained by the inclusion of animal models of traumatic head injuries in the analysis by Lukasiuk et al that we did not include. The justification for their inclusion is the initial hit theory whereby an early insult, be it ischemic, traumatic or infective, sets into motion a series of molecular changes that lead into the latency period before chronic epilepsy. However, recent figures suggest only 2% to 5% of traumatic brain injury cases will develop epilepsy (75) . Second, posttraumatic seizures are more commonly a result of cerebral contusions leading to scarring and altered neuronal circuitry rather than the classical MTLE syndrome. Filtering out the head injury papers from Lukasiuk et al's study leaves only four consistently regulated genes, three of which are included in our list of regulated genes (Gadd45a, Ctsd, Ctss, Zfp36). The last gene, zinc finger protein 36 (zfp36) is only reported differentially expressed in different arms of the same study by Becker et al and was excluded from our analysis. The complexity of neuronal structure and organization within the mesial temporal lobe regions may contribute to this issue. In particular, the anatomical subregions of the hippocampus demonstrate both histological and functional differences in their composition and response to certain conditions. Whereas CA1 and CA3 are considered integral to the transmission of input signals, CA2 is considered a transitional zone with no clear function and the dentate gyrus is considered the main input pathway into the hippocampus, receiving afferents itself from the entorhinal cortex via the perforant pathway (31) . Increasing interest in gene expression profiling between hippocampal subfields has suggested a molecular basis underlying the previously defined anatomic subregions of the hippocampus (112) . This may further improve understanding of the differing histopathological responses described earlier.