# Is Precision Therapy in Infantile-Onset Epileptic Encephalopathieshes Still Too Far to Call Upon?
## 1 Introduction  
Epileptic and developmental encephalopathies (EDEs) are severe neurological disorders marked by early-onset seizures, developmental delays, and cognitive and motor impairments [1]. These disorders, predominantly manifesting in infancy or early childhood, involve multisystemic complications including psychiatric, behavioral, sleep, gastrointestinal, musculoskeletal, and movement disorders [2]. Despite phenotypic similarities, EDEs are genetically heterogeneous, encompassing syndromes such as Early Myoclonic Encephalopathy, Ohtahara Syndrome, West Syndrome, and Dravet Syndrome [3]. Recentadvancements in molecular genetics, neurodiagnostic technologies including functional study such as molecular dynamics and patch clamps have refined our understanding of these disorders.  
Precision therapies have emerged as targeted approaches to address the root causes of specific EDEs, marking a pivotal shift from conventional treatments. For example, pyridoxine (Vitamin B6) is an effective treatment for pyridoxine-dependent epilepsy, a rare autosomal recessive disorder caused by mutations in the ALDH/A1 gene. Early administration of pyridoxine not only prevents seizures but also mitigates long-term neurodevelopmental damage [4]. Similarly, the ketogenic diet, a high-fat, low-carbohydrate dietary regimen, serves as a precision therapy for GLUT1 Deficiency Syndrome (GLUT1-DS) by providing ketones as an alternative energy source for the brain [5]. This diet has demonstrated remarkable efficacy in reducing seizure frequency and improving cognitive function, offering a tailored solution that directly targets the metabolic dysfunction underlying the condition.  
However, it is important to note that not all therapies classified as \"precision\" share the same degree of specificity or mechanistic insight [6]. While the ketogenic diet directly addresses the metabolic needs of GLUT1-DS patients by bypassing the impaired glucose transport system, it remains a broader intervention compared to gene-specific therapies, such as antisense oligonucleotides or CRISPR-based approaches targeting specific mutations [7]. Similarly, pyridoxine therapy, while life-changing for individuals with pyridoxine-dependent epilepsy, relies on metabolic supplementation rather than directly correcting the genetic mutation itself [8]. These examples illustrate that precision therapies can vary significantly in their level of refinement, ranging from metabolic interventions to advanced gene editing technologies.  
The aim of this perspective articles lies in its comprehensive exploration of the current state of precision therapy for EDEs, bridging the gap between emerging research and clinical application. By highlighting the potential and challenges of precision medicine, this work serves as a valuable resource for clinicians, researchers, and policymakers aiming to improve outcomes for individuals with these complex disorders. Moreover, it underscores the need for multidisciplinary collaboration and innovation to expand the scope of precision therapies, ensuring that advances in molecular and genetic science translate into tangible benefits for patients. This article not only emphasizes the transformative potential of precision medicine but also advocates for its integration into routine clinical practice, paving the way for a more tailored and effective approach to managing EDEs.