Their consistent dysregulation in epileptic tissues (e.g., ILF3-AS1↑ in TLE hippocampi, miR-155hg↑ in CSE) positions them not only as biomarkers but as master regulators of the “glial-RNA axis.” Therapeutic targeting of these nodes—via antisense oligonucleotides against H19/NEAT1 or engineered exosomes delivering UCA1/SNHG1 mimics—represents a promising paradigm for multitargeted intervention in drug-resistant epilepsy. This evidence concerns the gene NEAT1 and epilepsy.