In electrically non-excitable cells, calcium influx is essential for regulating a host of kinetically distinct processes involving exocytosis, enzyme control, gene regulation, cell growth and proliferation and apoptosis. The major calcium entry pathway in these cells is the store-operated one, in which the emptying of intracellular inositol trisphosphate-sensitive calcium stores activates calcium influx (store-operated calcium entry, or capacitative calcium entry). Several biophysically distinct store-operated currents have been reported, but the best characterized is the calcium release-activated calcium current, ICRAC. Here we show that calcium entry through CRAC channels is a key trigger for the generation of the intracellular messenger arachidonic acid via stimulation of calcium-dependent phospholipase A2, which is subsequently converted to the potent pro-inflammatory paracrine signal leukotriene C4 by the 5-lipoxygenase enzyme. The mechanism whereby calcium entry through CRAC channels activates calcium-dependent phospholipase A2 and 5lipoxygenase will be discussed,