Kv6.4, a voltage-gated potassium channel subunit, selectively regulates the firing patterns of parvalbumin-positive interneurons, the brain's primary inhibitory cells that maintain neural network stability. These fast-spiking neurons depend on Kv6.4 to modulate their electrical properties and sustained firing capacity during high-frequency activity periods. This discovery illuminates a previously unknown mechanism controlling one of the brain's most critical cell populations. Understanding inhibitory neuron regulation carries profound implications for neurological and psychiatric conditions. Parvalbumin interneurons dysfunction underlies schizophrenia, autism spectrum disorders, and epilepsy pathophysiology. The selective expression pattern suggests Kv6.4 could represent a precision therapeutic target without affecting other neuronal populations. However, this appears to be fundamental mechanistic research rather than translational work, likely conducted in animal models. The specificity of Kv6.4 to these particular interneurons offers insights into how the brain achieves cellular diversity through ion channel specialization. Future investigations should examine whether Kv6.4 variants correlate with inhibitory network disorders and whether pharmacological modulation could restore proper inhibitory balance in disease states.