Quite surprisingly, we found no difference in SOCE-induced mitochondrial Ca2+ transients between healthy and ALS astrocytes (Figure 5), suggesting that the mitochondrial Ca2+ buffering capacity plays no significant role in the excess of cytosolic Ca2+ accumulation observed in hSOD1(G93A) after SOCE stimulation. Here, SOD1 is linked to amyotrophic lateral sclerosis.