Absence seizures are generalized nonmotor epileptic events characterized by transient impairment of consciousness associated with generalized spike-and-wave discharges on electroencephalography (EEG). [1,2] Traditionally regarded as benign pediatric epileptic phenomena, contemporary evidence increasingly demonstrates that absence seizures comprise a heterogeneous neurobiological spectrum involving complex genetic, molecular, electrophysiological, and thalamocortical network abnormalities. [3,4] Although childhood absence epilepsy remains the prototypical syndrome, absence seizures also occur in juvenile absence epilepsy, juvenile myoclonic epilepsy, epilepsy with eyelid myoclonia, and several developmental and epileptic encephalopathies. [5,6] The pathogenesis of absence seizures involves pathological oscillatory synchronization within cortico-thalamo-cortical circuits mediated by abnormal γ-aminobutyric acid (GABAergic) neurotransmission, T-type calcium channel dysfunction, altered glutamatergic signaling, and genetically determined neuronal hyperexcitability. [4,7] Advances in molecular genetics have identified multiple susceptibility genes including CACNA1H, CACNG3, GABRG2, SLC2A1, SCN1A, and HCN1, thereby highlighting the polygenic and heterogeneous nature of generalized epileptogenesis. [8-10] Clinically, absence seizures manifest as sudden behavioral arrest, impaired awareness, staring episodes, automatisms, eyelid fluttering, and interruption of ongoing activity. [2] Despite their apparently subtle presentation, recurrent absence seizures may substantially impair academic performance, attention, psychosocial functioning, and neurocognitive development. [11] Diagnostic delays remain common because episodes are frequently misinterpreted as daydreaming, inattentiveness, behavioral disorders, or psychogenic events. [12] Electroencephalography remains the cornerstone of diagnosis, classically demonstrating bilateral synchronous 3-Hz generalized spike-and-wave discharges. [1] Contemporary management includes ethosuximide, valproate, and lamotrigine as first-line therapies, while emerging therapeutic research focuses on precision medicine, network neuromodulation, and molecular-targeted interventions. [13,14] This comprehensive descriptive review examines the genetics, molecular genetics, classifications, epidemiology, pathogenesis, clinical manifestations, diagnostic evaluation, differential diagnosis, treatment strategies, prognosis, contemporary controversies, research limitations, and future directions relating to absence seizures