Depleted ER Ca2+ causes extracellular Ca2+ entry, which is referred to as store-operated Ca2+ entry (SOCE).14,15 An increase in [Ca2+]i is essential for salivary fluid secretion, and impaired [Ca2+]i increase is associated with salivary hypofunction in patients with Sjögren’s Syndrome.16 Increased [Ca2+]i induces Cl− movement through the transmembrane protein 16A (TMEM16A) Ca2+-activated Cl− channel.17–19 The accumulation of Cl− in the lumen induces water movement through the aquaporin 5 (AQP5) water channel and tight junctions. Here, ANO1 is linked to Sjogren syndrome.