The endoplasmic reticulum (ER) Ca sensor STIM1, best-known for its essential role in triggering influx of extracellular Ca via Ca-release-activated channels when ER stores become depleted, unexpectedly also regulates Ca entry through voltage-gated Ca channels. In response to a drop in ER luminal Ca level, this ER membrane-spanning sensor can contact voltage-gated Ca channels in the plasma membrane and thereby inhibit Ca influx through them. This previously unappreciated, interaction between ER Ca level and magnitude of Ca influx via voltage-gated Ca channels may turn out to powerfully impact Ca signaling in excitable cells, including neurotransmitter release, structural and functional postsynaptic plasticity, and transcription factor translocation.