These results suggest that activation of some receptors (e.g., PAR-2) may recruit both ORAI1 and TRPC1 (although to a far lesser extent) to replenish depleted stores in MDA-MB-468 breast cancer cells, whereas other mechanisms are specific for ORAI1 over TRPC1, such as ATP and store-depletion as a consequence of SERCA inhibition. This evidence concerns the gene TRPC1 and breast cancer.