Although Kir4.1 potassium channels, a member of the family of inward rectifying K+ (Kir) channels, are predominantly responsible for maintaining the hyperpolarized membrane potential of astrocytes and in extracellular K+ buffering under normal conditions [2–5], members of the tandem pore family of K+ channels (such as TREK-1 and TREK-2 channels) have also been ascribed a role in this process, particularly during conditions of stress, such as during ischemia [6–10]. The gene discussed is KCNA3; the disease is ischemia.