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How might a cell modulate the signals it receives from other cells and from the environment, so that it would not get too wound up or even signaled to death? It uses negative feedback regulation, as any sensible machinery would. Given that two very basic ways of signaling are to raise the free Ca2+ concentration inside the cell ([Ca2+]i) and to alter the electrical potential across the cell membrane, it is no wonder that the large-conductance voltage- and Ca2+-dependent K+ (MaxiK) channels, which are negative feedback regulators for these signaling processes, are so prevalent in our nerves, muscles, secretory glands, and other eukaryotes, including protozoa (1). In this issue, Meera et al. (21) give us new insight into the molecular mechanisms through which the MaxiK channels respond to Ca2+ and membrane potential and thereby enhance our understanding of the control of electrical signaling.

Ways and means for left shifts in the MaxiK channel