ORAI1 and alkaline phosphatase measurement: - 33 The recognition of store-operated Ca2+ entry (SOCE) as a potential therapeutic target for AP dates back to as early as 2000.34 The pharmacological development of specific CRAC channel inhibitors for AP treatment has significantly expanded over recent years.35 The substantial therapeutic appeal of targeting CRAC channels is due to the dependence of intracellular protease activation on cytosolic Ca2+ overload, which occurs after abnormal Ca2+ depletion of the endoplasmic reticulum (ER) and excessive Orai1/CRAC channel-mediated Ca2+ entry.21,29,36- 38