KCNA6 encodes a voltage-gated potassium channel that mediates transmembrane potassium transport in excitable membranes by forming tetrameric channels through which potassium ions pass according to their electrochemical gradient. The channel alternates between open and closed states in response to membrane voltage and can form both homotetrameric and heterotetrameric assemblies with other Kv1 family members; channel properties depend on the composition of alpha subunits and are modulated by cytoplasmic beta subunits that regulate subcellular localization and promote rapid inactivation. De novo missense variants in KCNA6 cause early-onset developmental epileptic encephalopathy 1, with mutations in critical regions such as the selectivity filter and S6 hinge producing severe loss-of-function channel properties. Other variants show dominant gain-of-function effects that slow channel closure and shift voltage dependence of deactivation 2, indicating that both loss- and gain-of-function mutations may contribute to disease phenotypes. KCNA6 variants have also been associated with neurodevelopmental disorders and seizures with onset in infancy 2. Beyond neurological disease, KCNA6 has emerging roles in viral tropism—recent screening identified it as a host factor facilitating SARS-CoV-2 entry, with inhibitors of KCNA6 reducing viral infection 3. Pharmacological modulation of potassium channels, including compounds like dalfampridine and amifampridine, represents a therapeutic approach for channelopathies involving KCNA6.