## 1 Introduction  
It has been estimated that about 50 million people worldwide suffer from epilepsy [1]. In 2015, about 3.4 million people had active epilepsy in the U.S. alone [2]. Epilepsy is one of the most common and most disabling neurological disorders, characterized by recurrent unprovoked excessive brain activity [3]. The current understanding of the neurophysiological mechanisms of epilepsy is largely based on extensive investigations of neuronal cells. However, glial cells have also been demonstrated to play a fundamental role in triggering seizures. Accurate diagnosis of epilepsy is challenging and therapeutic strategies span a range from single, to multiple drug courses of administration, to respective neurosurgical procedures and dietary therapy. In spite of the fact that several dozen antiepileptic drugs (AEDs) are available, there are still approximately 20-30% of patients who do not respond satisfactorily to these AEDs [3]. To develop new, effective treatments, studies focus on the development of the central nervous system (CNS) and neuronal activities in vivo to understand the causes and mechanisms of the disease initiation and progression [4]. However, to find effective treatments for patients who are refractory to current AEDs, it is necessary to study each case more precisely and individually. Hippocampal biopsy tissue of pharmaco-resistant Temporal Lobe Epileptic (TLE) patients is an extraordinarily useful substrate to study molecular mechanisms related to structural and cellular abnormalities in epilepsy. Several genes and signaling cascade alterations have already been reported in the literature based on the TLE hippocampus analysis [5]. The availability of gene expression profiling provides a detailed insight into the disease for each individual patient. Methods, such as microarray and RNA sequencing, developed in the recent decade are used to obtain genome-wide mRNA expression data. One of the advantages of using such methods is that this type of investigation is biomarker driven. Especially with whole genome-wide data, the comprehensive information on the status of each functioning unit, its interacting complex and interaction pathways is suitable for analysis, which can reveal potentially important molecular mechanisms and novel therapeutic targets. By investigating genome-wide expression data, we can study the integrated results of all possible causative changes for each patient. Thus, the results of such an analysis are considered to be precise and biomarker-driven [6]. Epilepsy is a complex neuro-pathology that arises due to different etiologies, having various localizations, often occurring in conjunction with other diseases. Irrespective of what triggers the paroxysm, the electrical discharge during seizure is the common clinical manifestation for all forms of epilepsy, suggesting an underlying common molecular mechanism [7]. Although revealing the precise origin of epilepsy is still part of the ongoing investigations, it was shown that the cause may vary from de novo genetic mutations [8] to traumatic brain injury [9; 10]. While gene mutations may naturally lead to altered downstream pathway behavior, brain injury was also shown to cause chronically altered gene expression signatures of genes that were linked to epilepsy [9]. Recent studies revealed some genetic causes of epilepsy, such as gene SCN1A mutations, which affect sodium channels [8] and tuberous sclerosis complex (TSC) mutations, which lead to the dysregulation of the mechanistic target of rapamycin (mTOR) pathway [11], both of which lead to epileptic conditions. Mechanisms of epileptogenesis consist of genetic and epigenetic alterations occurring in both neuronal and astroglia cells [12]. Abnormal activity of astrocytes during epileptic events has been extensively reported to play a major role due to their K+ buffering role in the extracellular milieu [13]. Clinical diagnosis of epilepsy starts with an identification of the type of seizure and proceeds with EEG and neuroimaging studies.