Recent studies have determined that K+ channel gene expression is dynamically controlled in endocrine, cardiac, and neuronal cells. This regulation is induced by physiological stimuli (e.g., hormones, transmitters, depolarization), drugs (e.g., opiates) and with pathophysiological conditions (e.g., seizures, hypertension). In many cases, alterations in subunit expression are driven by transcriptional changes. Furthermore, resultant changes in excitability can be produced within hours because of the rapid turnover of Kv-channel proteins. Finally, the consequences of altering K+-channel subunit are complex because a single gene product can participate in forming functionally distinct homomeric and heteromeric channels in the same cell. Thus, regulating K+-channel genes constitutes a novel mechanism for producing intricate long-term changes in excitability.