Immunoreceptor signalling leads to Ca²⁺ release from intracellular stores, which is followed by the entry of external Ca²⁺ into the cell through mysterious store-operated Ca²⁺ (SOC) channels. Recent studies have identified stromal interaction molecules (STIMs) as having an essential role in SOC influx. Remarkably, Ca²⁺ store depletion induces a rapid redistribution of the endoplasmic reticulum STIM1 into puncta that accumulate near the plasma membrane. The combined data suggest that STIM1 functions as a Ca²⁺ sensor in the signalling pathways connecting Ca²⁺ store depletion to SOC entry.