Summarizing, our results indicate that STIM1 N-linked glycosylation plays a relevant role in the activation of TG-evoked SOCE in non-tumoral breast epithelial cells but, by contrast, STIM1 glycosylation is without effect in the regulation of Ca2+ influx in breast cancer cells, an adaptative mechanism that might play an important role in apoptosis resistance in breast tumoral cells, as the lack of sensitivity of SOCE to STIM1 glycosylation in breast cancer cells deprives the apoptotic event of a regulatory mechanism. Here, STIM1 is linked to breast cancer.