Finally, we suggest that store-operated Ca2+ entry (SOCE) is over-activated in patients suffering from stroke/ictus, as revealed by the increase in the STIM1/Orai1 interaction found under resting conditions and, further, because MEG-01 cells transfected with siRNA STC2 to evoke artificial reduction in the STC2 expression presented an increased SOCE with respect to the control cells transfected with siRNA A. Conversely, the expression of the non-capacitative Ca2+ channels, Orai3 and TRPC6, was found to be reduced in patients with stroke. The gene discussed is STC2; the disease is stroke disorder.